document_title: HIV/AIDS

question_text: the virus of aids affects the growth of

question_tokens: the virus of aids affects the growth of

text: HIV/AIDS

text: Signs and symptoms

text: There are three main stages of HIV infection: acute infection, clinical latency and AIDS.[1]

text: Acute infection

text: The initial period following the contraction of HIV is called acute HIV, primary HIV or acute retroviral syndrome.[2][26] Many individuals develop an influenza-like illness or a mononucleosis-like illness 2–4 weeks post exposure while others have no significant symptoms.[27][28] Symptoms occur in 40–90% of cases and most commonly include fever, large tender lymph nodes, throat inflammation, a rash, headache, and/or sores of the mouth and genitals.[26][28] The rash, which occurs in 20–50% of cases, presents itself on the trunk and is maculopapular, classically.[29] Some people also develop opportunistic infections at this stage.[26] Gastrointestinal symptoms, such as vomiting or diarrhea may occur.[28] Neurological symptoms of peripheral neuropathy or Guillain–Barré syndrome also occurs.[28] The duration of the symptoms varies, but is usually one or two weeks.[28]

text: Due to their nonspecific character, these symptoms are not often recognized as signs of HIV infection. Even cases that do get seen by a family doctor or a hospital are often misdiagnosed as one of the many common infectious diseases with overlapping symptoms. Thus, it is recommended that HIV be considered in people presenting an unexplained fever who may have risk factors for the infection.[28]

text: Clinical latency

text: The initial symptoms are followed by a stage called clinical latency, asymptomatic HIV, or chronic HIV.[1] Without treatment, this second stage of the natural history of HIV infection can last from about three years[30] to over 20 years[31] (on average, about eight years).[32] While typically there are few or no symptoms at first, near the end of this stage many people experience fever, weight loss, gastrointestinal problems and muscle pains.[1] Between 50 and 70% of people also develop persistent generalized lymphadenopathy, characterized by unexplained, non-painful enlargement of more than one group of lymph nodes (other than in the groin) for over three to six months.[2]

text: Although most HIV-1 infected individuals have a detectable viral load and in the absence of treatment will eventually progress to AIDS, a small proportion (about 5%) retain high levels of CD4+ T cells (T helper cells) without antiretroviral therapy for more than 5 years.[28][33] These individuals are classified as HIV controllers or long-term nonprogressors (LTNP).[33] Another group consists of those who maintain a low or undetectable viral load without anti-retroviral treatment, known as "elite controllers" or "elite suppressors". They represent approximately 1 in 300 infected persons.[34]

text: Acquired immunodeficiency syndrome

text: Acquired immunodeficiency syndrome (AIDS) is defined in terms of either a CD4+ T cell count below 200 cells per µL or the occurrence of specific diseases in association with an HIV infection.[28] In the absence of specific treatment, around half of people infected with HIV develop AIDS within ten years.[28] The most common initial conditions that alert to the presence of AIDS are pneumocystis pneumonia (40%), cachexia in the form of HIV wasting syndrome (20%), and esophageal candidiasis.[28] Other common signs include recurring respiratory tract infections.[28]

text: Opportunistic infections may be caused by bacteria, viruses, fungi, and parasites that are normally controlled by the immune system.[35] Which infections occur depends partly on what organisms are common in the person's environment.[28] These infections may affect nearly every organ system.[36]

text: People with AIDS have an increased risk of developing various viral-induced cancers, including Kaposi's sarcoma, Burkitt's lymphoma, primary central nervous system lymphoma, and cervical cancer.[29] Kaposi's sarcoma is the most common cancer occurring in 10 to 20% of people with HIV.[37] The second most common cancer is lymphoma, which is the cause of death of nearly 16% of people with AIDS and is the initial sign of AIDS in 3 to 4%.[37] Both these cancers are associated with human herpesvirus 8.[37] Cervical cancer occurs more frequently in those with AIDS because of its association with human papillomavirus (HPV).[37] Conjunctival cancer (of the layer that lines the inner part of eyelids and the white part of the eye) is also more common in those with HIV.[38]

text: Additionally, people with AIDS frequently have systemic symptoms such as prolonged fevers, sweats (particularly at night), swollen lymph nodes, chills, weakness, and unintended weight loss.[39] Diarrhea is another common symptom, present in about 90% of people with AIDS.[40] They can also be affected by diverse psychiatric and neurological symptoms independent of opportunistic infections and cancers.[41]

text: Transmission

text:
Average per act risk of getting HIV
by exposure route to an infected source

Exposure route
Chance of infection

Blood transfusion
90%[42]

Childbirth (to child)
25%[43]

Needle-sharing injection drug use
0.67%[42]

Percutaneous needle stick
0.30%[44]

Receptive anal intercourse*
0.04–3.0%[45]

Insertive anal intercourse*
0.03%[46]

Receptive penile-vaginal intercourse*
0.05–0.30%[45][47]

Insertive penile-vaginal intercourse*
0.01–0.38%[45][47]

Receptive oral intercourse*§
0–0.04%[45]

Insertive oral intercourse*§
0–0.005%[48]

* assuming no condom use
§ source refers to oral intercourse
performed on a man

text: HIV is transmitted by three main routes: sexual contact, significant exposure to infected body fluids or tissues, and from mother to child during pregnancy, delivery, or breastfeeding (known as vertical transmission).[12] There is no risk of acquiring HIV if exposed to feces, nasal secretions, saliva, sputum, sweat, tears, urine, or vomit unless these are contaminated with blood.[49] It is possible to be co-infected by more than one strain of HIV—a condition known as HIV superinfection.[50]

text: Sexual

text: The most frequent mode of transmission of HIV is through sexual contact with an infected person.[12] Globally, the most common mode of HIV transmission is via sexual contacts between people of the opposite sex;[12] however, the pattern of transmission varies among countries. As of 2014, most HIV transmission in the United States occurred among men who had sex with men (83% of new HIV diagnoses among males aged 13 and older and 67% of total new diagnoses).[51] In the US, gay and bisexual men aged 13 to 24 accounted for an estimated 92% of new HIV diagnoses among all men in their age group and 27% of new diagnoses among all gay and bisexual men.[51] About 15% of gay and bisexual men have HIV while 28 percent of transgender women test positive in the US.[51][52]

text: With regard to unprotected heterosexual contacts, estimates of the risk of HIV transmission per sexual act appear to be four to ten times higher in low-income countries than in high-income countries.[53] In low-income countries, the risk of female-to-male transmission is estimated as 0.38% per act, and of male-to-female transmission as 0.30% per act; the equivalent estimates for high-income countries are 0.04% per act for female-to-male transmission, and 0.08% per act for male-to-female transmission.[53] The risk of transmission from anal intercourse is especially high, estimated as 1.4–1.7% per act in both heterosexual and homosexual contacts.[53][54] While the risk of transmission from oral sex is relatively low, it is still present.[55] The risk from receiving oral sex has been described as "nearly nil";[56] however, a few cases have been reported.[57] The per-act risk is estimated at 0–0.04% for receptive oral intercourse.[58] In settings involving prostitution in low income countries, risk of female-to-male transmission has been estimated as 2.4% per act and male-to-female transmission as 0.05% per act.[53]

text: Risk of transmission increases in the presence of many sexually transmitted infections[59] and genital ulcers.[53] Genital ulcers appear to increase the risk approximately fivefold.[53] Other sexually transmitted infections, such as gonorrhea, chlamydia, trichomoniasis, and bacterial vaginosis, are associated with somewhat smaller increases in risk of transmission.[58]

text: The viral load of an infected person is an important risk factor in both sexual and mother-to-child transmission.[60] During the first 2.5 months of an HIV infection a person's infectiousness is twelve times higher due to this high viral load.[58] If the person is in the late stages of infection, rates of transmission are approximately eightfold greater.[53] An HIV-positive person who has an undetectable viral load as a result of long-term treatment has effectively no risk of transmitting HIV sexually.[61]

text: Commercial sex workers (including those in pornography) have an increased rate of HIV.[62][63] Rough sex can be a factor associated with an increased risk of transmission.[64] Sexual assault is also believed to carry an increased risk of HIV transmission as condoms are rarely worn, physical trauma to the vagina or rectum is likely, and there may be a greater risk of concurrent sexually transmitted infections.[65]

text: Body fluids

text: The second most frequent mode of HIV transmission is via blood and blood products.[12] Blood-borne transmission can be through needle-sharing during intravenous drug use, needle stick injury, transfusion of contaminated blood or blood product, or medical injections with unsterilized equipment. The risk from sharing a needle during drug injection is between 0.63 and 2.4% per act, with an average of 0.8%.[66] The risk of acquiring HIV from a needle stick from an HIV-infected person is estimated as 0.3% (about 1 in 333) per act and the risk following mucous membrane exposure to infected blood as 0.09% (about 1 in 1000) per act.[49] In the United States intravenous drug users made up 12% of all new cases of HIV in 2009,[67] and in some areas more than 80% of people who inject drugs are HIV positive.[12]

text: HIV is transmitted in about 93% of blood transfusions using infected blood.[66] In developed countries the risk of acquiring HIV from a blood transfusion is extremely low (less than one in half a million) where improved donor selection and HIV screening is performed;[12] for example, in the UK the risk is reported at one in five million[68] and in the United States it was one in 1.5 million in 2008.[69] In low income countries, only half of transfusions may be appropriately screened (as of 2008),[70] and it is estimated that up to 15% of HIV infections in these areas come from transfusion of infected blood and blood products, representing between 5% and 10% of global infections.[12][71] Although rare because of screening, it is possible to acquire HIV from organ and tissue transplantation.[72]

text: Unsafe medical injections play a significant role in HIV spread in sub-Saharan Africa. In 2007, between 12 and 17% of infections in this region were attributed to medical syringe use.[73] The World Health Organization estimates the risk of transmission as a result of a medical injection in Africa at 1.2%.[73] Significant risks are also associated with invasive procedures, assisted delivery, and dental care in this area of the world.[73]

text: People giving or receiving tattoos, piercings, and scarification are theoretically at risk of infection but no confirmed cases have been documented.[74] It is not possible for mosquitoes or other insects to transmit HIV.[75]

text: Mother-to-child

text: HIV can be transmitted from mother to child during pregnancy, during delivery, or through breast milk, resulting in the baby also contracting HIV.[76][77] This is the third most common way in which HIV is transmitted globally.[12] In the absence of treatment, the risk of transmission before or during birth is around 20% and in those who also breastfeed 35%.[77] As of 2008, vertical transmission accounted for about 90% of cases of HIV in children.[77] With appropriate treatment the risk of mother-to-child infection can be reduced to about 1%.[77] Preventive treatment involves the mother taking antiretrovirals during pregnancy and delivery, an elective caesarean section, avoiding breastfeeding, and administering antiretroviral drugs to the newborn.[78] Antiretrovirals when taken by either the mother or the infant decrease the risk of transmission in those who do breastfeed.[79] However, many of these measures are not available in the developing world.[78] If blood contaminates food during pre-chewing it may pose a risk of transmission.[74]

text: If a woman is untreated, two years of breastfeeding results in an HIV/AIDS risk in her baby of about 17%. Treatment decreases this risk to 1 to 2% per year. Due to the increased risk of death without breastfeeding in many areas in the developing world, the World Health Organization recommends either: (1) the mother and baby being treated with antiretroviral medication while breastfeeding being continued (2) the provision of safe formula.[80] Infection with HIV during pregnancy is also associated with miscarriage.[81]

text: Virology

text: HIV is the cause of the spectrum of disease known as HIV/AIDS. HIV is a retrovirus that primarily infects components of the human immune system such as CD4+ T cells, macrophages and dendritic cells. It directly and indirectly destroys CD4+ T cells.[82]

text: HIV is a member of the genus Lentivirus,[83] part of the family Retroviridae.[84] Lentiviruses share many morphological and biological characteristics. Many species of mammals are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period.[85] Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry into the target cell, the viral RNA genome is converted (reverse transcribed) into double-stranded DNA by a virally encoded reverse transcriptase that is transported along with the viral genome in the virus particle. The resulting viral DNA is then imported into the cell nucleus and integrated into the cellular DNA by a virally encoded integrase and host co-factors.[86] Once integrated, the virus may become latent, allowing the virus and its host cell to avoid detection by the immune system.[87] Alternatively, the virus may be transcribed, producing new RNA genomes and viral proteins that are packaged and released from the cell as new virus particles that begin the replication cycle anew.[88]

text: HIV is now known to spread between CD4+ T cells by two parallel routes: cell-free spread and cell-to-cell spread, i.e. it employs hybrid spreading mechanisms.[89] In the cell-free spread, virus particles bud from an infected T cell, enter the blood/extracellular fluid and then infect another T cell following a chance encounter.[89] HIV can also disseminate by direct transmission from one cell to another by a process of cell-to-cell spread.[90][91] The hybrid spreading mechanisms of HIV contribute to the virus's ongoing replication against antiretroviral therapies.[89][92]

text: Two types of HIV have been characterized: HIV-1 and HIV-2. HIV-1 is the virus that was originally discovered (and initially referred to also as LAV or HTLV-III). It is more virulent, more infective,[93] and is the cause of the majority of HIV infections globally. The lower infectivity of HIV-2 as compared with HIV-1 implies that fewer people exposed to HIV-2 will be infected per exposure. Because of its relatively poor capacity for transmission, HIV-2 is largely confined to West Africa.[94]

text: Pathophysiology

text: After the virus enters the body there is a period of rapid viral replication, leading to an abundance of virus in the peripheral blood. During primary infection, the level of HIV may reach several million virus particles per milliliter of blood.[95] This response is accompanied by a marked drop in the number of circulating CD4+ T cells. The acute viremia is almost invariably associated with activation of CD8+ T cells, which kill HIV-infected cells, and subsequently with antibody production, or seroconversion. The CD8+ T cell response is thought to be important in controlling virus levels, which peak and then decline, as the CD4+ T cell counts recover. A good CD8+ T cell response has been linked to slower disease progression and a better prognosis, though it does not eliminate the virus.[96]

text: Ultimately, HIV causes AIDS by depleting CD4+ T cells. This weakens the immune system and allows opportunistic infections. T cells are essential to the immune response and without them, the body cannot fight infections or kill cancerous cells. The mechanism of CD4+ T cell depletion differs in the acute and chronic phases.[97] During the acute phase, HIV-induced cell lysis and killing of infected cells by cytotoxic T cells accounts for CD4+ T cell depletion, although apoptosis may also be a factor. During the chronic phase, the consequences of generalized immune activation coupled with the gradual loss of the ability of the immune system to generate new T cells appear to account for the slow decline in CD4+ T cell numbers.[98]

text: Although the symptoms of immune deficiency characteristic of AIDS do not appear for years after a person is infected, the bulk of CD4+ T cell loss occurs during the first weeks of infection, especially in the intestinal mucosa, which harbors the majority of the lymphocytes found in the body.[99] The reason for the preferential loss of mucosal CD4+ T cells is that the majority of mucosal CD4+ T cells express the CCR5 protein which HIV uses as a co-receptor to gain access to the cells, whereas only a small fraction of CD4+ T cells in the bloodstream do so.[100] A specific genetic change that alters the CCR5 protein when present in both chromosomes very effectively prevents HIV-1 infection.[101]

text: HIV seeks out and destroys CCR5 expressing CD4+ T cells during acute infection.[102] A vigorous immune response eventually controls the infection and initiates the clinically latent phase. CD4+ T cells in mucosal tissues remain particularly affected.[102] Continuous HIV replication causes a state of generalized immune activation persisting throughout the chronic phase.[103] Immune activation, which is reflected by the increased activation state of immune cells and release of pro-inflammatory cytokines, results from the activity of several HIV gene products and the immune response to ongoing HIV replication. It is also linked to the breakdown of the immune surveillance system of the gastrointestinal mucosal barrier caused by the depletion of mucosal CD4+ T cells during the acute phase of disease.[104]

text: Diagnosis

text: HIV/AIDS is diagnosed via laboratory testing and then staged based on the presence of certain signs or symptoms.[26] HIV screening is recommended by the United States Preventive Services Task Force for all people 15 years to 65 years of age including all pregnant women.[105] Additionally, testing is recommended for those at high risk, which includes anyone diagnosed with a sexually transmitted illness.[29] In many areas of the world, a third of HIV carriers only discover they are infected at an advanced stage of the disease when AIDS or severe immunodeficiency has become apparent.[29]

text: HIV testing

text: Most people infected with HIV develop specific antibodies (i.e. seroconvert) within three to twelve weeks of the initial infection.[28] Diagnosis of primary HIV before seroconversion is done by measuring HIV-RNA or p24 antigen.[28] Positive results obtained by antibody or PCR testing are confirmed either by a different antibody or by PCR.[26]

text: Antibody tests in children younger than 18 months are typically inaccurate due to the continued presence of maternal antibodies.[106] Thus HIV infection can only be diagnosed by PCR testing for HIV RNA or DNA, or via testing for the p24 antigen.[26] Much of the world lacks access to reliable PCR testing and many places simply wait until either symptoms develop or the child is old enough for accurate antibody testing.[106] In sub-Saharan Africa as of 2007–2009 between 30 and 70% of the population were aware of their HIV status.[107] In 2009, between 3.6 and 42% of men and women in Sub-Saharan countries were tested[107] which represented a significant increase compared to previous years.[107]

text: Classifications

text: Two main clinical staging systems are used to classify HIV and HIV-related disease for surveillance purposes: the WHO disease staging system for HIV infection and disease,[26] and the CDC classification system for HIV infection.[108] The CDC's classification system is more frequently adopted in developed countries. Since the WHO's staging system does not require laboratory tests, it is suited to the resource-restricted conditions encountered in developing countries, where it can also be used to help guide clinical management. Despite their differences, the two systems allow comparison for statistical purposes.[2][26][108]

text: The World Health Organization first proposed a definition for AIDS in 1986.[26] Since then, the WHO classification has been updated and expanded several times, with the most recent version being published in 2007.[26] The WHO system uses the following categories:

text:
Primary HIV infection: May be either asymptomatic or associated with acute retroviral syndrome.[26]
Stage I: HIV infection is asymptomatic with a CD4+ T cell count (also known as CD4 count) greater than 500 per microlitre (µl or cubic mm) of blood.[26] May include generalized lymph node enlargement.[26]
Stage II: Mild symptoms which may include minor mucocutaneous manifestations and recurrent upper respiratory tract infections. A CD4 count of less than 500/µl.[26]
Stage III: Advanced symptoms which may include unexplained chronic diarrhea for longer than a month, severe bacterial infections including tuberculosis of the lung, and a CD4 count of less than 350/µl.[26]
Stage IV or AIDS: severe symptoms which include toxoplasmosis of the brain, candidiasis of the esophagus, trachea, bronchi or lungs and Kaposi's sarcoma. A CD4 count of less than 200/µl.[26]

text: The United States Center for Disease Control and Prevention also created a classification system for HIV, and updated it in 2008 and 2014.[108][109] This system classifies HIV infections based on CD4 count and clinical symptoms, and describes the infection in five groups.[109] In those greater than six years of age it is:[109]

text:
Stage 0: the time between a negative or indeterminate HIV test followed less than 180 days by a positive test
Stage 1: CD4 count ≥ 500 cells/µl and no AIDS defining conditions
Stage 2: CD4 count 200 to 500 cells/µl and no AIDS defining conditions
Stage 3: CD4 count ≤ 200 cells/µl or AIDS defining conditions
Unknown: if insufficient information is available to make any of the above classifications

text: For surveillance purposes, the AIDS diagnosis still stands even if, after treatment, the CD4+ T cell count rises to above 200 per µL of blood or other AIDS-defining illnesses are cured.[2]

text: Prevention

text: Sexual contact

text: Consistent condom use reduces the risk of HIV transmission by approximately 80% over the long term.[110] When condoms are used consistently by a couple in which one person is infected, the rate of HIV infection is less than 1% per year.[111] There is some evidence to suggest that female condoms may provide an equivalent level of protection.[112] Application of a vaginal gel containing tenofovir (a reverse transcriptase inhibitor) immediately before sex seems to reduce infection rates by approximately 40% among African women.[113] By contrast, use of the spermicide nonoxynol-9 may increase the risk of transmission due to its tendency to cause vaginal and rectal irritation.[114]

text: Circumcision in Sub-Saharan Africa "reduces the acquisition of HIV by heterosexual men by between 38% and 66% over 24 months".[115] Due to these studies, both the World Health Organization and UNAIDS recommended male circumcision as a method of preventing female-to-male HIV transmission in 2007 in areas with a high rates of HIV.[116] However, whether it protects against male-to-female transmission is disputed,[117][118] and whether it is of benefit in developed countries and among men who have sex with men is undetermined.[119][120][121] The International Antiviral Society, however, does recommend for all sexually active heterosexual males and that it be discussed as an option with men who have sex with men.[122] Some experts fear that a lower perception of vulnerability among circumcised men may cause more sexual risk-taking behavior, thus negating its preventive effects.[123]

text: Programs encouraging sexual abstinence do not appear to affect subsequent HIV risk.[124] Evidence of any benefit from peer education is equally poor.[125] Comprehensive sexual education provided at school may decrease high risk behavior.[126][127] A substantial minority of young people continues to engage in high-risk practices despite knowing about HIV/AIDS, underestimating their own risk of becoming infected with HIV.[128] Voluntary counseling and testing people for HIV does not affect risky behavior in those who test negative but does increase condom use in those who test positive.[129] It is not known whether treating other sexually transmitted infections is effective in preventing HIV.[59]

text: Pre-exposure

text: Antiretroviral treatment among people with HIV whose CD4 count ≤ 550 cells/µL is a very effective way to prevent HIV infection of their partner (a strategy known as treatment as prevention, or TASP).[130] TASP is associated with a 10 to 20 fold reduction in transmission risk.[130][131] Pre-exposure prophylaxis (PrEP) with a daily dose of the medications tenofovir, with or without emtricitabine, is effective in a number of groups including men who have sex with men, couples where one is HIV positive, and young heterosexuals in Africa.[113] It may also be effective in intravenous drug users with a study finding a decrease in risk of 0.7 to 0.4 per 100 person years.[132]

text: Universal precautions within the health care environment are believed to be effective in decreasing the risk of HIV.[133] Intravenous drug use is an important risk factor and harm reduction strategies such as needle-exchange programs and opioid substitution therapy appear effective in decreasing this risk.[134][135]

text: Post-exposure

text: A course of antiretrovirals administered within 48 to 72 hours after exposure to HIV-positive blood or genital secretions is referred to as post-exposure prophylaxis (PEP).[136] The use of the single agent zidovudine reduces the risk of a HIV infection five-fold following a needle-stick injury.[136] As of 2013, the prevention regimen recommended in the United States consists of three medications—tenofovir, emtricitabine and raltegravir—as this may reduce the risk further.[137]

text: PEP treatment is recommended after a sexual assault when the perpetrator is known to be HIV positive, but is controversial when their HIV status is unknown.[138] The duration of treatment is usually four weeks[139] and is frequently associated with adverse effects—where zidovudine is used, about 70% of cases result in adverse effects such as nausea (24%), fatigue (22%), emotional distress (13%) and headaches (9%).[49]

text: Mother-to-child

text: Programs to prevent the vertical transmission of HIV (from mothers to children) can reduce rates of transmission by 92–99%.[77][134] This primarily involves the use of a combination of antiviral medications during pregnancy and after birth in the infant and potentially includes bottle feeding rather than breastfeeding.[77][140] If replacement feeding is acceptable, feasible, affordable, sustainable, and safe, mothers should avoid breastfeeding their infants; however exclusive breastfeeding is recommended during the first months of life if this is not the case.[141] If exclusive breastfeeding is carried out, the provision of extended antiretroviral prophylaxis to the infant decreases the risk of transmission.[142] In 2015, Cuba became the first country in the world to eradicate mother-to-child transmission of HIV.[143]

text: Vaccination

text: Currently, there is no licensed vaccine for HIV or AIDS.[7] The most effective vaccine trial to date, RV 144, was published in 2009 and found a partial reduction in the risk of transmission of roughly 30%, stimulating some hope in the research community of developing a truly effective vaccine.[144] Further trials of the RV 144 vaccine are ongoing.[145][146]

text: Treatment

text: There is currently no cure or effective HIV vaccine. Treatment consists of highly active antiretroviral therapy (HAART) which slows progression of the disease.[147] As of 2010 more than 6.6 million people were taking them in low and middle income countries.[148] Treatment also includes preventive and active treatment of opportunistic infections.

text: Antiviral therapy

text: Current HAART options are combinations (or "cocktails") consisting of at least three medications belonging to at least two types, or "classes," of antiretroviral agents.[149] Initially treatment is typically a non-nucleoside reverse transcriptase inhibitor (NNRTI) plus two nucleoside analog reverse transcriptase inhibitors (NRTIs).[150] Typical NRTIs include: zidovudine (AZT) or tenofovir (TDF) and lamivudine (3TC) or emtricitabine (FTC).[150] Combinations of agents which include protease inhibitors (PI) are used if the above regimen loses effectiveness.[149]

text: The World Health Organization and United States recommends antiretrovirals in people of all ages including pregnant women as soon as the diagnosis is made regardless of CD4 count.[14][122][151] Once treatment is begun it is recommended that it is continued without breaks or "holidays".[29] Many people are diagnosed only after treatment ideally should have begun.[29] The desired outcome of treatment is a long term plasma HIV-RNA count below 50 copies/mL.[29] Levels to determine if treatment is effective are initially recommended after four weeks and once levels fall below 50 copies/mL checks every three to six months are typically adequate.[29] Inadequate control is deemed to be greater than 400 copies/mL.[29] Based on these criteria treatment is effective in more than 95% of people during the first year.[29]

text: Benefits of treatment include a decreased risk of progression to AIDS and a decreased risk of death.[152] In the developing world treatment also improves physical and mental health.[153] With treatment there is a 70% reduced risk of acquiring tuberculosis.[149] Additional benefits include a decreased risk of transmission of the disease to sexual partners and a decrease in mother-to-child transmission.[149][154] The effectiveness of treatment depends to a large part on compliance.[29] Reasons for non-adherence include poor access to medical care,[155] inadequate social supports, mental illness and drug abuse.[156] The complexity of treatment regimens (due to pill numbers and dosing frequency) and adverse effects may reduce adherence.[157] Even though cost is an important issue with some medications,[158] 47% of those who needed them were taking them in low and middle income countries as of 2010[148] and the rate of adherence is similar in low-income and high-income countries.[159]

text: Specific adverse events are related to the antiretroviral agent taken.[160] Some relatively common adverse events include: lipodystrophy syndrome, dyslipidemia, and diabetes mellitus, especially with protease inhibitors.[2] Other common symptoms include diarrhea,[160][161] and an increased risk of cardiovascular disease.[162] Newer recommended treatments are associated with fewer adverse effects.[29] Certain medications may be associated with birth defects and therefore may be unsuitable for women hoping to have children.[29]

text: Treatment recommendations for children are somewhat different from those for adults. The World Health Organization recommends treating all children less than 5 years of age; children above 5 are treated like adults.[163] The United States guidelines recommend treating all children less than 12 months of age and all those with HIV RNA counts greater than 100,000 copies/mL between one year and five years of age.[164]

text: Opportunistic infections

text: Measures to prevent opportunistic infections are effective in many people with HIV/AIDS. In addition to improving current disease, treatment with antiretrovirals reduces the risk of developing additional opportunistic infections.[160] Adults and adolescents who are living with HIV (even on anti-retroviral therapy) with no evidence of active tuberculosis in settings with high tuberculosis burden should receive isoniazid preventive therapy (IPT), the tuberculin skin test can be used to help decide if IPT is needed.[165] Vaccination against hepatitis A and B is advised for all people at risk of HIV before they become infected; however it may also be given after infection.[166] Trimethoprim/sulfamethoxazole prophylaxis between four and six weeks of age and ceasing breastfeeding in infants born to HIV positive mothers is recommended in resource limited settings.[167] It is also recommended to prevent PCP when a person's CD4 count is below 200 cells/uL and in those who have or have previously had PCP.[168] People with substantial immunosuppression are also advised to receive prophylactic therapy for toxoplasmosis and MAC.[169] Appropriate preventive measures have reduced the rate of these infections by 50% between 1992 and 1997.[170] Influenza vaccination and pneumococcal polysaccharide vaccine are often recommended in people with HIV/AIDS with some evidence of benefit.[171][172]

text: Diet

text: The World Health Organization (WHO) has issued recommendations regarding nutrient requirements in HIV/AIDS.[173] A generally healthy diet is promoted. Dietary intake of micronutrients at RDA levels by HIV-infected adults is recommended by the WHO; higher intake of vitamin A, zinc, and iron can produce adverse effects in HIV positive adults, and is not recommended unless there is documented deficiency.[173][174][175][176] Dietary supplementation for people who are infected with HIV and who have inadequate nutrition or dietary deficiencies may strengthen their immune systems or help them recover from infections, however evidence indicating an overall benefit in morbidity or reduction in mortality is not consistent.[177]

text: Evidence for supplementation with selenium is mixed with some tentative evidence of benefit.[178] For pregnant and lactating women with HIV, multivitamin supplement improves outcomes for both mothers and children.[179] If the pregnant or lactating mother has been advised to take anti-retroviral medication to prevent mother-to-child HIV transmission, multivitamin supplements should not replace these treatments.[179] There is some evidence that vitamin A supplementation in children with an HIV infection reduces mortality and improves growth.[180]

text: Alternative medicine

text: In the US, approximately 60% of people with HIV use various forms of complementary or alternative medicine,[181] even though the effectiveness of most of these therapies has not been established.[182] There is not enough evidence to support the use of herbal medicines.[183] There is insufficient evidence to recommend or support the use of medical cannabis to try to increase appetite or weight gain.[184]

text: Prognosis

text: HIV/AIDS has become a chronic rather than an acutely fatal disease in many areas of the world.[185] Prognosis varies between people, and both the CD4 count and viral load are useful for predicted outcomes.[28] Without treatment, average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.[15] After the diagnosis of AIDS, if treatment is not available, survival ranges between 6 and 19 months.[186][187] HAART and appropriate prevention of opportunistic infections reduces the death rate by 80%, and raises the life expectancy for a newly diagnosed young adult to 20–50 years.[185][188][189] This is between two thirds[188] and nearly that of the general population.[29][190] If treatment is started late in the infection, prognosis is not as good:[29] for example, if treatment is begun following the diagnosis of AIDS, life expectancy is ~10–40 years.[29][185] Half of infants born with HIV die before two years of age without treatment.[167]

text:
no data
  ≤ 10
  10–25
  25–50
  50–100

  100–500
  500–1000
  1,000–2,500
  2,500–5,000
  5,000–7500

  7,500–10,000
  10,000–50,000
  ≥ 50,000

text: The primary causes of death from HIV/AIDS are opportunistic infections and cancer, both of which are frequently the result of the progressive failure of the immune system.[170][191] Risk of cancer appears to increase once the CD4 count is below 500/μL.[29] The rate of clinical disease progression varies widely between individuals and has been shown to be affected by a number of factors such as a person's susceptibility and immune function;[192] their access to health care, the presence of co-infections;[186][193] and the particular strain (or strains) of the virus involved.[194][195]

text: Tuberculosis co-infection is one of the leading causes of sickness and death in those with HIV/AIDS being present in a third of all HIV-infected people and causing 25% of HIV-related deaths.[196] HIV is also one of the most important risk factors for tuberculosis.[197] Hepatitis C is another very common co-infection where each disease increases the progression of the other.[198] The two most common cancers associated with HIV/AIDS are Kaposi's sarcoma and AIDS-related non-Hodgkin's lymphoma.[191] Other cancers that are more frequent include anal cancer, Burkitt's lymphoma, primary central nervous system lymphoma, and cervical cancer.[29][199]

text: Even with anti-retroviral treatment, over the long term HIV-infected people may experience neurocognitive disorders,[200] osteoporosis,[201] neuropathy,[202] cancers,[203][204] nephropathy,[205] and cardiovascular disease.[161] Some conditions like lipodystrophy may be caused both by HIV and its treatment.[161]

text: Epidemiology

text:
No data
  <0.10
  0.10–0.5
  0.5–1

  1–5
  5–15
  15–50

text: HIV/AIDS is a global pandemic.[207] As of 2016, approximately 36.7 million people have HIV worldwide with the number of new infections that year being about 1.8 million.[16] This is down from 3.1 million new infections in 2001.[208] Slightly over half the infected population are women and 2.1 million are children.[16] It resulted in about 1 million deaths in 2016, down from a peak of 1.9 million in 2005.[16]

text: Sub-Saharan Africa is the region most affected. In 2010, an estimated 68% (22.9 million) of all HIV cases and 66% of all deaths (1.2 million) occurred in this region.[209] This means that about 5% of the adult population is infected[210] and it is believed to be the cause of 10% of all deaths in children.[211] Here in contrast to other regions women compose nearly 60% of cases.[209] South Africa has the largest population of people with HIV of any country in the world at 5.9 million.[209] Life expectancy has fallen in the worst-affected countries due to HIV/AIDS; for example, in 2006 it was estimated that it had dropped from 65 to 35 years in Botswana.[19] Mother-to-child transmission, as of 2013, in Botswana and South Africa has decreased to less than 5% with improvement in many other African nations due to improved access to antiretroviral therapy.[212]

text: South & South East Asia is the second most affected; in 2010 this region contained an estimated 4 million cases or 12% of all people living with HIV resulting in approximately 250,000 deaths.[210] Approximately 2.4 million of these cases are in India.[209]

text: In 2008 in the United States approximately 1.2 million people were living with HIV, resulting in about 17,500 deaths. The US Centers for Disease Control and Prevention estimated that in 2008 20% of infected Americans were unaware of their infection.[213] As of 2016 about 675,000 people have died of HIV/AIDS in the USA since the beginning of the HIV epidemic.[52] In the United Kingdom as of 2015 there were approximately 101,200 cases which resulted in 594 deaths.[214] In Canada as of 2008 there were about 65,000 cases causing 53 deaths.[215] Between the first recognition of AIDS in 1981 and 2009 it has led to nearly 30 million deaths.[216] Prevalence is lowest in Middle East and North Africa at 0.1% or less, East Asia at 0.1% and Western and Central Europe at 0.2%.[210] The worst affected European countries, in 2009 and 2012 estimates, are Russia, Ukraine, Latvia, Moldova, Portugal and Belarus, in decreasing order of prevalence.[217]

text: History

text: Discovery

text: AIDS was first clinically observed in 1981 in the United States.[37] The initial cases were a cluster of injecting drug users and homosexual men with no known cause of impaired immunity who showed symptoms of Pneumocystis carinii pneumonia (PCP), a rare opportunistic infection that was known to occur in people with very compromised immune systems.[218] Soon thereafter, an unexpected number of homosexual men developed a previously rare skin cancer called Kaposi's sarcoma (KS).[219][220] Many more cases of PCP and KS emerged, alerting U.S. Centers for Disease Control and Prevention (CDC) and a CDC task force was formed to monitor the outbreak.[221]

text: In the early days, the CDC did not have an official name for the disease, often referring to it by way of the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus.[222][223] They also used Kaposi's sarcoma and opportunistic infections, the name by which a task force had been set up in 1981.[224] At one point, the CDC coined the phrase "the 4H disease", since the syndrome seemed to affect heroin users, homosexuals, hemophiliacs, and Haitians.[225][226] In the general press, the term "GRID", which stood for gay-related immune deficiency, had been coined.[227] However, after determining that AIDS was not isolated to the gay community,[224] it was realized that the term GRID was misleading and the term AIDS was introduced at a meeting in July 1982.[228] By September 1982 the CDC started referring to the disease as AIDS.[229]

text: In 1983, two separate research groups led by Robert Gallo and Luc Montagnier declared that a novel retrovirus may have been infecting people with AIDS, and published their findings in the same issue of the journal Science.[230][231] Gallo claimed that a virus his group had isolated from a person with AIDS was strikingly similar in shape to other human T-lymphotropic viruses (HTLVs) his group had been the first to isolate. Gallo's group called their newly isolated virus HTLV-III. At the same time, Montagnier's group isolated a virus from a person presenting with swelling of the lymph nodes of the neck and physical weakness, two characteristic symptoms of AIDS. Contradicting the report from Gallo's group, Montagnier and his colleagues showed that core proteins of this virus were immunologically different from those of HTLV-I. Montagnier's group named their isolated virus lymphadenopathy-associated virus (LAV).[221] As these two viruses turned out to be the same, in 1986, LAV and HTLV-III were renamed HIV.[232]

text: Origins

text: Both HIV-1 and HIV-2 are believed to have originated in non-human primates in West-central Africa and were transferred to humans in the early 20th century.[20] HIV-1 appears to have originated in southern Cameroon through the evolution of SIV(cpz), a simian immunodeficiency virus (SIV) that infects wild chimpanzees (HIV-1 descends from the SIVcpz endemic in the chimpanzee subspecies Pan troglodytes troglodytes).[233][234] The closest relative of HIV-2 is SIV(smm), a virus of the sooty mangabey (Cercocebus atys atys), an Old World monkey living in coastal West Africa (from southern Senegal to western Côte d'Ivoire).[94] New World monkeys such as the owl monkey are resistant to HIV-1 infection, possibly because of a genomic fusion of two viral resistance genes.[235] HIV-1 is thought to have jumped the species barrier on at least three separate occasions, giving rise to the three groups of the virus, M, N, and O.[236]

text: There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat vendors, commonly acquire SIV.[237] However, SIV is a weak virus which is typically suppressed by the human immune system within weeks of infection. It is thought that several transmissions of the virus from individual to individual in quick succession are necessary to allow it enough time to mutate into HIV.[238] Furthermore, due to its relatively low person-to-person transmission rate, SIV can only spread throughout the population in the presence of one or more high-risk transmission channels, which are thought to have been absent in Africa before the 20th century.

text: Specific proposed high-risk transmission channels, allowing the virus to adapt to humans and spread throughout the society, depend on the proposed timing of the animal-to-human crossing. Genetic studies of the virus suggest that the most recent common ancestor of the HIV-1 M group dates back to circa 1910.[239] Proponents of this dating link the HIV epidemic with the emergence of colonialism and growth of large colonial African cities, leading to social changes, including a higher degree of sexual promiscuity, the spread of prostitution, and the accompanying high frequency of genital ulcer diseases (such as syphilis) in nascent colonial cities.[240] While transmission rates of HIV during vaginal intercourse are low under regular circumstances, they are increased many fold if one of the partners suffers from a sexually transmitted infection causing genital ulcers. Early 1900s colonial cities were notable due to their high prevalence of prostitution and genital ulcers, to the degree that, as of 1928, as many as 45% of female residents of eastern Kinshasa were thought to have been prostitutes, and, as of 1933, around 15% of all residents of the same city had syphilis.[240]

text: An alternative view holds that unsafe medical practices in Africa after World War II, such as unsterile reuse of single use syringes during mass vaccination, antibiotic and anti-malaria treatment campaigns, were the initial vector that allowed the virus to adapt to humans and spread.[238][241][242]

text: The earliest well-documented case of HIV in a human dates back to 1959 in the Congo.[243] The earliest retrospectively described case of AIDS is believed to have been in Norway beginning in 1966.[244] In July 1960, in the wake its independence, the United Nations recruited Francophone experts and technicians from all over the world to assist in filling administrative gaps left by Belgium, who did not leave behind an African elite to run the country. By 1962, Haitians made up the second largest group of well-educated experts (out of the 48 national groups recruited), that totaled around 4500 in the country.[245][246] Dr. Jacques Pépin, a Quebecer author of The Origins of AIDS, stipulates that Haiti was one of HIV's entry points to the United States and that one of them may have carried HIV back across the Atlantic in the 1960s.[246] Although the virus may have been present in the United States as early as 1966,[247] the vast majority of infections occurring outside sub-Saharan Africa (including the U.S.) can be traced back to a single unknown individual who became infected with HIV in Haiti and then brought the infection to the United States some time around 1969.[248] The epidemic then rapidly spread among high-risk groups (initially, sexually promiscuous men who have sex with men). By 1978, the prevalence of HIV-1 among homosexual male residents of New York City and San Francisco was estimated at 5%, suggesting that several thousand individuals in the country had been infected.[248]

text: Society and culture

text: Stigma

text: AIDS stigma exists around the world in a variety of ways, including ostracism, rejection, discrimination and avoidance of HIV infected people; compulsory HIV testing without prior consent or protection of confidentiality; violence against HIV infected individuals or people who are perceived to be infected with HIV; and the quarantine of HIV infected individuals.[22] Stigma-related violence or the fear of violence prevents many people from seeking HIV testing, returning for their results, or securing treatment, possibly turning what could be a manageable chronic illness into a death sentence and perpetuating the spread of HIV.[250]

text: AIDS stigma has been further divided into the following three categories:

text:
Instrumental AIDS stigma—a reflection of the fear and apprehension that are likely to be associated with any deadly and transmissible illness.[251]
Symbolic AIDS stigma—the use of HIV/AIDS to express attitudes toward the social groups or lifestyles perceived to be associated with the disease.[251]
Courtesy AIDS stigma—stigmatization of people connected to the issue of HIV/AIDS or HIV-positive people.[252]

text: Often, AIDS stigma is expressed in conjunction with one or more other stigmas, particularly those associated with homosexuality, bisexuality, promiscuity, prostitution, and intravenous drug use.[253]

text: In many developed countries, there is an association between AIDS and homosexuality or bisexuality, and this association is correlated with higher levels of sexual prejudice, such as anti-homosexual/bisexual attitudes.[254] There is also a perceived association between AIDS and all male-male sexual behavior, including sex between uninfected men.[251] However, the dominant mode of spread worldwide for HIV remains heterosexual transmission.[255]

text: In 2003, as part of an overall reform of marriage and population legislation, it became legal for people with AIDS to marry in China.[256]

text: In 2013 the U.S. National Library of Medicine developed a traveling exhibition titled, "Surviving and Thriving: AIDS, Politics, and Culture",[257] covering medical research, U.S. government's response, and personal stories from people with AIDS, caregivers, and activists.[258]

text: Economic impact

text: HIV/AIDS affects the economics of both individuals and countries.[211] The gross domestic product of the most affected countries has decreased due to the lack of human capital.[211][259] Without proper nutrition, health care and medicine, large numbers of people die from AIDS-related complications. They will not only be unable to work, but will also require significant medical care. It is estimated that as of 2007 there were 12 million AIDS orphans.[211] Many are cared for by elderly grandparents.[260]

text: Returning to work after beginning treatment for HIV/AIDS is difficult, and affected people often work less than the average worker. Unemployment in people with HIV/AIDS also is associated with suicidal ideation, memory problems, and social isolation; employment increases self-esteem, sense of dignity, confidence, and quality of life. A 2015 Cochrane review found low-quality evidence that antiretroviral treatment helps people with HIV/AIDS work more, and increases the chance that a person with HIV/AIDS will be employed.[261]

text: By affecting mainly young adults, AIDS reduces the taxable population, in turn reducing the resources available for public expenditures such as education and health services not related to AIDS resulting in increasing pressure for the state's finances and slower growth of the economy. This causes a slower growth of the tax base, an effect that is reinforced if there are growing expenditures on treating the sick, training (to replace sick workers), sick pay and caring for AIDS orphans. This is especially true if the sharp increase in adult mortality shifts the responsibility and blame from the family to the government in caring for these orphans.[260]

text: At the household level, AIDS causes both loss of income and increased spending on healthcare. A study in Côte d'Ivoire showed that households having a person with HIV/AIDS spent twice as much on medical expenses as other households. This additional expenditure also leaves less income to spend on education and other personal or family investment.[262]

text: Religion and AIDS

text: The topic of religion and AIDS has become highly controversial in the past twenty years, primarily because some religious authorities have publicly declared their opposition to the use of condoms.[263][264] The religious approach to prevent the spread of AIDS according to a report by American health expert Matthew Hanley titled The Catholic Church and the Global AIDS Crisis argues that cultural changes are needed including a re-emphasis on fidelity within marriage and sexual abstinence outside of it.[264]

text: Some religious organizations have claimed that prayer can cure HIV/AIDS. In 2011, the BBC reported that some churches in London were claiming that prayer would cure AIDS, and the Hackney-based Centre for the Study of Sexual Health and HIV reported that several people stopped taking their medication, sometimes on the direct advice of their pastor, leading to a number of deaths.[265] The Synagogue Church Of All Nations advertised an "anointing water" to promote God's healing, although the group denies advising people to stop taking medication.[265]

text: Media portrayal

text: One of the first high-profile cases of AIDS was the American Rock Hudson, a gay actor who had been married and divorced earlier in life, who died on October 2, 1985 having announced that he was suffering from the virus on July 25 that year. He had been diagnosed during 1984.[266] A notable British casualty of AIDS that year was Nicholas Eden, a gay politician and son of the late prime minister Anthony Eden.[267] On November 24, 1991, the virus claimed the life of British rock star Freddie Mercury, lead singer of the band Queen, who died from an AIDS-related illness having only revealed the diagnosis on the previous day.[268] However, he had been diagnosed as HIV positive in 1987.[269] One of the first high-profile heterosexual cases of the virus was Arthur Ashe, the American tennis player. He was diagnosed as HIV positive on August 31, 1988, having contracted the virus from blood transfusions during heart surgery earlier in the 1980s. Further tests within 24 hours of the initial diagnosis revealed that Ashe had AIDS, but he did not tell the public about his diagnosis until April 1992.[270] He died as a result on February 6, 1993 at age 49.[271]

text: Therese Frare's photograph of gay activist David Kirby, as he lay dying from AIDS while surrounded by family, was taken in April 1990. LIFE magazine said the photo became the one image "most powerfully identified with the HIV/AIDS epidemic." The photo was displayed in LIFE magazine, was the winner of the World Press Photo, and acquired worldwide notoriety after being used in a United Colors of Benetton advertising campaign in 1992.[272] In 1996, Johnson Aziga, a Ugandan-born Canadian was diagnosed with HIV, but subsequently had unprotected sex with 11 women without disclosing his diagnosis. By 2003 seven had contracted HIV, and two died from complications related to AIDS.[273][274] Aziga was convicted of first-degree murder and was sentenced for life.[275]

text: Criminal transmission

text: Criminal transmission of HIV is the intentional or reckless infection of a person with the human immunodeficiency virus (HIV). Some countries or jurisdictions, including some areas of the United States, have laws that criminalize HIV transmission or exposure.[276] Others may charge the accused under laws enacted before the HIV pandemic.

text: Misconceptions

text: There are many misconceptions about HIV and AIDS. Three of the most common are that AIDS can spread through casual contact, that sexual intercourse with a virgin will cure AIDS,[277][278][279] and that HIV can infect only gay men and drug users. In 2014, some among the British public wrongly thought one could get HIV from kissing (16%), sharing a glass (5%), spitting (16%), a public toilet seat (4%), and coughing or sneezing (5%).[280] Other misconceptions are that any act of anal intercourse between two uninfected gay men can lead to HIV infection, and that open discussion of HIV and homosexuality in schools will lead to increased rates of AIDS.[281][282]

text: A small group of individuals continue to dispute the connection between HIV and AIDS,[283] the existence of HIV itself, or the validity of HIV testing and treatment methods.[284][285] These claims, known as AIDS denialism, have been examined and rejected by the scientific community.[286] However, they have had a significant political impact, particularly in South Africa, where the government's official embrace of AIDS denialism (1999–2005) was responsible for its ineffective response to that country's AIDS epidemic, and has been blamed for hundreds of thousands of avoidable deaths and HIV infections.[287][288][289]

text: Several discredited conspiracy theories have held that HIV was created by scientists, either inadvertently or deliberately. Operation INFEKTION was a worldwide Soviet active measures operation to spread the claim that the United States had created HIV/AIDS. Surveys show that a significant number of people believed – and continue to believe – in such claims.[290]

text: Research

text: HIV/AIDS research includes all medical research which attempts to prevent, treat, or cure HIV/AIDS along with fundamental research about the nature of HIV as an infectious agent and AIDS as the disease caused by HIV.

text: Many governments and research institutions participate in HIV/AIDS research. This research includes behavioral health interventions such as sex education, and drug development, such as research into microbicides for sexually transmitted diseases, HIV vaccines, and antiretroviral drugs. Other medical research areas include the topics of pre-exposure prophylaxis, post-exposure prophylaxis, and circumcision and HIV.


document_title: Economic planning

question_text: the basic aim of economic planning in india is promoting

root

text: Economic planning

text: Socialist economic planning[edit]

text:
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text: Different forms of economic planning have been featured in various models of socialism. These range from decentralized-planning systems, which are based on collective decision-making and disaggregated information, to centralized systems of planning conducted by technical experts who use aggregated information to formulate plans of production. In a fully developed socialist economy, engineers and technical specialists, overseen or appointed in a democratic manner, would coordinate the economy in terms of physical units without any need or use for financial-based calculation. The economy of the Soviet Union never reached this stage of development, so planned its economy in financial terms throughout the duration of its existence.[5] Nonetheless, a number of alternative metrics were developed for assessing the performance of non-financial economies in terms of physical output (i.e.: net material product versus gross domestic product).

tag: p

text: In general, the various models of socialist economic planning exist as theoretical constructs that have not been implemented fully by any economy, partially because they depend on vast changes on a global scale (see: mode of production). In the context of mainstream economics and the field of comparative economic systems, "socialist planning" usually refers to the Soviet-type command economy, regardless of whether or not this economic system actually constituted a type of socialism or state capitalism or a third, non-socialist and non-capitalist type of system.

text: In some models of socialism, economic planning completely substitutes the market mechanism, supposedly rendering monetary relations and the price system obsolete. In other models, planning is utilized as a complement to markets.

text: Concept of socialist planning[edit]

text: The classical conception of socialist economic planning held by Marxists involved an economic system where goods and services were valued, demanded and produced directly for their use-value, as opposed to being produced as a by-product of the pursuit of profit by business enterprises. This idea of "production for use" is a fundamental aspect of a socialist economy. This involves social control over the allocation of the surplus product, and in its most extensive theoretical form, calculation-in-kind in place of financial calculation. For Marxists in particular, planning entails control of the surplus product (profit) by the associated producers in a democratic manner.[6] This differs from planning within the framework of capitalism, which is based on the planned accumulation of capital in order to either stabilize the business cycle (when undertaken by governments) or to maximize profits (when undertaken by firms), as opposed to the socialist concept of planned production for use.

text: In such a socialist society based on economic planning, the primary function of the state apparatus changes from one of political rule over people (via the creation and enforcement of laws) into a technical administration of production, distribution and organization; that is the state would become a coordinating economic entity rather than a mechanism of political and class-based control, thereby ceasing to be a state in the traditional sense.[7]

text: Planning versus Command[edit]

text: The concept of a command economy is differentiated from the concept of a planned economy (or economic planning), especially by socialists and Marxists, who liken command economies (such as that of the former Soviet Union) to that of a single capitalist firm, organized in a top-down administrative fashion based on bureaucratic organization akin to that of a capitalist corporation.[8]

text: Economic analysts have argued that the economy of the former Soviet Union actually represented an administered or command economy as opposed to a planned economy because planning did not play an operational role in the allocation of resources among productive units in the economy; in actuality, the main allocation mechanism was a system of command-and-control. As a result, the phrase administrative command economy gained currency as a more accurate descriptor of Soviet-type economies.[9]

text: Decentralized planning[edit]

text: Decentralized economic planning is a planning process that starts at the user-level in a bottom-up flow of information. As such, decentralized planning often appears as a complement to the idea of socialist self-management (most notably by libertarian socialists and democratic socialists).

text: The theoretical postulates for models of decentralized socialist planning stem from the thought of Karl Kautsky, Rosa Luxemburg, Nikolai Bukharin and Oskar Lange.[10] This model involves economic decision-making based on self-governance from the bottom-up (by employees and consumers) without any directing central authority. This often contrasts with the doctrine of orthodox Marxist-Leninism, which advocates directive administrative planning where directives are passed down from higher authorities (planning agencies) to agents (enterprise managers), who in turn give orders to workers.

text: Two contemporary models of decentralized planning are Participatory economics, developed by the economist Michael Albert; and negotiated coordination, developed by the economist Pat Devine.

text: Material balances[edit]

text: Material balance planning was the type of economic planning employed by Soviet-type economies. This system emerged in a haphazard manner during the collectivisation drive under Joseph Stalin, and emphasized rapid growth and industrialization over efficiency. Eventually this method became an established part of the Soviet conception of "socialism" in the post-war period, and other Socialist states emulated it in the latter half of the 20th century. Material balancing involves a planning agency (Gosplan in the case of the USSR) taking a survey of available inputs and raw materials, using a balance-sheet to balance them with output targets specified by industry, thereby achieving a balance of supply and demand.[11]>

text: Lange-Lerner-Taylor model[edit]

text: The economic models developed in the 1920s and 1930s by American economists Fred M. Taylor and Abba Lerner, and by Polish economist Oskar Lange, involved a form of planning based on marginal cost pricing. In Lange's model, a central planning board would set prices for producer goods through a trial-and-error method, adjusting until the price matched the marginal cost, with the aim of achieving Pareto-efficient outcomes. Although these models were often described as "market socialism", they actually represented a form of "market simulation" planning.

text: Planning in capitalism[edit]

text: Intra-firm and intra-industry planning[edit]

text: Large corporations use planning to allocate resources internally among its divisions and subsidiaries. Many modern firms also utilize regression analysis to measure market demand in order to adjust prices and to decide upon the optimal quantities of output to be supplied. Planned obsolescence is often cited as a form of economic planning employed by large firms to increase demand for future products by deliberately limiting the operational lifespan of its products.

text: The internal structures of corporations have been described as centralized command economies that employ both planning and hierarchical organization and management. According to J. Bradford DeLong, a significant portion of transactions in Western economies do not pass through anything resembling a market. Many transactions are actually movements of value among different branches and divisions within corporations, companies and agencies. Furthermore, a significant portion of economic activity is planned in a centralized manner by managers within firms in the form of production planning and marketing management where consumer demand is estimated, targeted and included in the firm's overall plan; and in the form of production planning.[12]

text: In The New Industrial State, the American economist John Kenneth Galbraith posited that large firms manage both their prices and consumer demand for their products through sophisticated statistical methods. Galbraith also pointed out that, because of the increasingly complex nature of technology and specialization of knowledge, management had become increasingly specialized and bureaucratized. The internal structures of corporations and companies had been transformed into what he called a "technostructure", where specialized groups and committees are the primary decision-makers, and specialized managers, directors and financial advisers operate under formal bureaucratic procedures, replacing the individual entrepreneur's role (see also: Intrapreneurship). He states that both the obsolete notion of "entrepreneurial capitalism" and democratic socialism (defined as democratic management) are impossible organizational forms for managing a modern industrial system.[13]

text: Joseph Schumpeter, an economist associated with the Austrian school and Institutional school of economics, argued that the changing nature of economic activity – specifically the increasing bureaucratization and specialization required in production and management – was the major reason for why capitalism would eventually evolve into socialism. The role of the businessman was increasingly bureaucratic, and specific functions within the firm required increasingly specialized knowledge which could just as easily be supplied by state functionaries in publicly owned enterprises.

text: In the first volume of Capital, Karl Marx identified the process of capital accumulation as central to the law of motion of capitalism. Increased industrial capacity from increasing returns to scale further socializes production. Capitalism eventually socializes labor and production to a point where the traditional notions of private ownership and commodity production become increasingly insufficient for further expanding the productive capacities of society,[14] necessitating the emergence of a socialist economy where the means of production are socially owned and the surplus value is controlled by the workforce.[15] Many socialists viewed these tendencies, specifically the increasing trend toward economic planning in capitalist firms, as evidence of the increasing obsolescence of capitalism and inapplicability of ideals like perfect competition to the economy; with the next stage of evolution being the application of society-wide economic planning.

text: State development planning[edit]

text: State development planning or national planning refers to macroeconomic policies and financial planning conducted by governments to stabilize the market or promote economic growth in market-based economies. This involves the use of monetary policy, industrial policy and fiscal policy to "steer" the market toward targeted outcomes. Industrial policy includes government taking measures "aimed at improving the competitiveness and capabilities of domestic firms and promoting structural transformation."[16]

text: In contrast to socialist planning, state development planning does not replace the market mechanism and does not eliminate the use of money in production. It only applies to privately owned and publicly owned firms in the strategic sectors of the economy and seeks to coordinate their activities through indirect means and market-based incentives (such as tax breaks or subsidies).

text: In practice[edit]

text: Soviet Union[edit]

text: The Soviet model of economic planning is an economic system where decisions regarding production and investment are embodied in a plan formulated by Gosplan (State planning agency) through the process of material balances. Economic information, including consumer demand and enterprise resource requirements, are aggregated and used to balance supply (from available resource inventories) with demand (based on requirements for individual economic units and enterprises) through a system of iterations.

text: The Soviet economy operated in a centralized and hierarchical manner where directives were issued to lower-level organizations. As a result, the Soviet economic model was often referred to as a command economy or an administered economy because plan directives were enforced through inducements in a vertical power-structure, where planning played little functional role in the allocation of resources.[9]

text: United States[edit]

text: The United States utilized economic planning during the First World War. The Federal Government supplemented the price system with centralized resource allocation and created a number of new agencies to direct important economic sectors; notably the Food Administration, Fuel Administration, Railroad Administration and War Industries Board.[17] During the Second World War, the economy experienced staggering growth under a similar system of planning. In the postwar period, US governments utilized such measures as the Economic Stabilization Program to directly intervene in the economy to control prices, wages, etc. in different economic sectors.

text: From the start of the Cold War and up until the present day, the United States Federal Government has directed a significant amount of investment and funding into research and development (R&D), often initially through the Department of Defense. The government performs 50% of all R&D in the United States,[18] with a dynamic state-directed public-sector developing most of the technology that later becomes the basis of the private sector economy. As a result, Noam Chomsky has referred to the United States economic model as a form of State Capitalism.[19] Examples include laser technology, the internet, nanotechnology, telecommunications and computers, with most basic research and downstream commercialization financed by the public sector. This includes research in other fields including healthcare and energy, with 75% of most innovative drugs financed through the National Institutes of Health.[20]

text: East Asian Tigers[edit]

text: The development models of the East Asian Tiger economies involved varying degrees of economic planning and state-directed investment in a model sometimes described as "state development capitalism" or the "East Asian Model".

text: The governments of Malaysia and South Korea instituted a series of macroeconomic plans (First Malaysia Plan and Five-Year Plans of South Korea) to rapidly develop and industrialize their mixed economies.

text: The economy of Singapore was partially based on economic planning involving an active government industrial policy and high levels of state-owned industry in a free-market economy.

text: France[edit]

text: Under dirigisme, France utilized indicative planning and established a number of state-owned enterprises in strategic sectors of the economy. The concept behind indicative planning is the early identification of oversupply, bottlenecks and shortages so that state investment behavior can be modified in a timely fashion to reduce the incidence of market disequilibrium, with the goal of sustaining stable economic development and growth. Under this system France experienced its "Trente Glorieuses" period of economic prosperity.

text: Great Britain[edit]

text: The need for long-term economic planning to promote efficiency was a central component of Labour Party thinking down to the 1970s. The Conservative Party largely agreed, thus producing the Post-war consensus or broad bipartisan agreement on major policies.[21]

text: Criticisms[edit]

text: The most notable critique of economic planning came from Austrian economists Friedrich Hayek and Ludwig von Mises. Hayek argued that central planners could not possibly accrue the necessary information to formulate an effective plan for production because they are not exposed to the rapid changes in the particular time and place that take place in an economy, and are unfamiliar with these circumstances. The process of transmitting all the necessary information to planners is therefore inefficient.[22]

text: Proponents of decentralized economic planning have also criticized central economic planning. For example, Leon Trotsky believed that central planners, regardless of their intellectual capacity, operated without the input and participation of the millions of people who participate in the economy, and would therefore be unable to respond to local conditions quickly enough to effectively coordinate all economic activity.[23]


document_title: Entamoeba histolytica

question_text: where is entamoeba histolytica found in the body

text: Entamoeba histolytica

text: Transmission[edit]

text: The active (trophozoite) stage exists only in the host and in fresh loose feces; cysts survive outside the host in water, in soils, and on foods, especially under moist conditions on the latter. The infection can occur when a person puts anything into their mouth that has touched the feces of a person who is infected with E. histolytica, swallows something, such as water or food, that is contaminated with E. histolytica, or swallows E. histolytica cysts (eggs) picked up from contaminated surfaces or fingers.[3] The cysts are readily killed by heat and by freezing temperatures, and survive for only a few months outside of the host.[4] When cysts are swallowed they cause infections by excysting (releasing the trophozoite stage) in the digestive tract. The pathogenic nature of E. histolytica was first reported by Lösch in 1875, but it was not given its Latin name until Fritz Schaudinn described it in 1903. E. histolytica, as its name suggests (histo–lytic = tissue destroying), is pathogenic; infection can be asymptomatic or can lead to amoebic dysentery or amoebic liver abscess.[1][5] Symptoms can include fulminating dysentery, bloody diarrhea, weight loss, fatigue, abdominal pain, and amoeboma. The amoeba can actually 'bore' into the intestinal wall, causing lesions and intestinal symptoms, and it may reach the blood stream. From there, it can reach different vital organs of the human body, usually the liver, but sometimes the lungs, brain, spleen, etc. A common outcome of this invasion of tissues is a liver abscess, which can be fatal if untreated. Ingested red blood cells are sometimes seen in the amoeba cell cytoplasm.

text: Risk factors[edit]

text: Poor sanitary conditions are known to increase the risk of contracting amebiasis E. hystolytica.[6] In the United States, there is a much higher rate of amebiasis-related mortality in California and Texas, which might be caused by the proximity of those states to E. histolytica-endemic areas, such as Mexico, other parts of Latin America, and Asia.[7] E. hystolytica is also recognized as an emerging sexually transmissible pathogen, especially in male homosexual relations, causing outbreaks in non-endemic regions.[8] As such, high-risk sex behaviour is also a potential source of infection.[9] Although it is unclear whether there is a causal link, studies indicate a higher chance of being infected with E. hystolytica if one is also infected with HIV.[10][11]

text: Genome[edit]

text: The E. histolytica genome was sequenced, assembled, and automatically annotated in 2005.[12] The genome was reassembled and reannotated in 2010.[13] The 20 million basepair genome assembly contains 8,160 predicted genes; known and novel transposable elements have been mapped and characterized, functional assignments have been revised and updated, and additional information has been incorporated, including metabolic pathways, Gene Ontology assignments, curation of transporters, and generation of gene families.[14] The major group of transposable elements in E. histolytica are non-LTR retrotransposons. These have been divided in three families called EhLINEs and EhSINEs (EhLINE1,2,3 and EhSINE1,2,3).[15] EhLINE1 encode an endonuclease (EN) protein (in addition to reverse transcriptase and nucleotide-binding ORF1), which have similarity with bacterial restriction endonuclease. This similarity with bacterial protein indicates that transposable elements have been acquired from prokaryotes by horizontal gene transfer in this protozoan parasite.[16]

text: Pathology[edit]

text: In the vast majority of cases, infection is asymptomatic and the carrier is unaware they are infected. However, in an estimated 10% of cases E. histolytica causes disease. Once the trophozoites are excysted they colonize the large bowel, remaining on the surface of the mucus layer and feeding on bacteria and food particles. Occasionally, and in response to unknown stimuli, trophozoites move through the mucus layer where they come in contact with the epithelial cell layer and start the pathological process. E. histolytica has a lectin that binds to galactose and N-acetylgalactosamine sugars on the surface of the epithelial cells, The lectin normally is used to bind bacteria for ingestion. The parasite has several enzymes such as pore forming proteins, lipases, and cysteine proteases, which are normally used to digest bacteria in food vacuoles but which can cause lysis of the epithelial cells by inducing cellular necrosis and apoptosis when the trophozoite comes in contact with them and binds via the lectin. Enzymes released allow penetration into intestinal wall and blood vessels, sometimes on to liver and other organs.[17] The trophozoites will then ingest these dead cells. This damage to the epithelial cell layer attracts human immune cells and these in turn can be lysed by the trophozoite, which releases the immune cell's own lytic enzymes into the surrounding tissue, creating a type of chain reaction and leading to tissue destruction. This destruction manifests itself in the form of an 'ulcer' in the tissue, typically described as flask-shaped because of its appearance in transverse section. This tissue destruction can also involve blood vessels leading to bloody diarrhea, amebic dysentery. Occasionally, trophozoites enter the bloodstream where they are transported typically to the liver via the portal system. In the liver a similar pathological sequence ensues, leading to amebic liver abscesses. The trophozoites can also end up in other organs, sometimes via the bloodstream, sometimes via liver abscess rupture or fistulas. In all locations, similar pathology can occur.

text: Pathogen interaction[edit]

text: E. histolytica may modulate the virulence of certain human viruses and is itself a host for its own viruses.

text: For example, AIDS accentuates the damage and pathogenicity of E. histolytica.[11] On the other hand, cells infected with HIV are often consumed by E. histolytica. Infective HIV remains viable within the amoeba, although there has been no proof of human reinfection from amoeba carrying this virus.[18]

text: A burst of research on viruses of E. histolytica stems from a series of papers published by Diamond et al. from 1972 to 1979. In 1972, they hypothesized two separate polyhedral and filamentous viral strains within E. histolytica that caused cell lysis. Perhaps the most novel observation was that two kinds of viral strains existed, and that within one type of amoeba (strain HB-301) the polyhedral strain had no detrimental effect but led to cell lysis in another (strain HK-9). Although Mattern et al. attempted to explore the possibility that these protozoal viruses could function like bacteriophages, they found no significant changes in Entamoeba histolytica virulence when infected by viruses. However, no newer published research has been conducted on this species since.[19]

text: Diagnosis[edit]

text: Diagnosis is confirmed by microscopic examination for trophozoites or cysts in fresh or suitably preserved faecal specimens, smears of aspirates or scrapings obtained by proctoscopy, and aspirates of abscesses or other tissue specimen. A blood test is also available but is only recommended when a healthcare provider believes the infection may have spread beyond the intestine (gut) to some other organ of the body, such as the liver. However, this blood test may not be helpful in diagnosing current illness because the test can be positive if the patient has had amebiasis in the past, even if they are not infected at present.[20]

text:
Amoebic intestinal ulcer caused by E. histolytica

Trophozoites of E. histolytica with ingested erythrocytes

E. histolytica cyst

Immature E. histolytica cyst (mature cysts have 4 nuclei)

Multiplication by binary fission

E. hystolytica drawing

tag: ul

text: Treatment[edit]

text: There are a number of effective medications. Generally several antibiotics are available to treat entamoeba histolytica. The infected individual will be treated with only one antibiotic if the E. histolytica infection has not made the person sick and most likely be prescribed with two antibiotics if the person has been feeling sick.[21] Otherwise, below are other options for treatments.

text: Intestinal infection: Usually nitroimidazole derivatives are used because they are highly effective against the trophozoite form of the amoeba. Since they have little effect on amoeba cysts, usually this treatment is followed by an agent (such as paromomycin or diloxanide furoate) that acts on the organism in the lumen.

text: Liver abscess: In addition to targeting organisms in solid tissue, primarily with drugs like metronidazole and chloroquine, treatment of liver abscess must include agents that act in the lumen of the intestine (as in the preceding paragraph) to avoid re-invasion. Surgical drainage is usually not necessary except when rupture is imminent.[22]

text: People without symptoms: For people without symptoms (otherwise known as carriers, with no symptoms), non endemic areas should be treated by paromomycin, and other treatments include diloxanide furoate and iodoquinol.[citation needed] There have been problems with the use of iodoquinol and iodochlorhydroxyquin, so their use is not recommended. Diloxanide furoate can also be used by mildly symptomatic persons who are just passing cysts.

text:
Genus and species
Entamoeba histolytica

Etiologic agent of:
Amoebiasis; amoebic dysentery; extraintestinal amoebiasis, usually amoebic liver abscess; "anchovy sauce"); amoeba cutis; amoebic lung abscess ("liver-colored sputum")

Infective stage
Tetranucleated cyst (having 2-4 nuclei)

Definitive host
Human

Portal of entry
Mouth

Mode of transmission
Ingestion of mature cyst through contaminated food or water

Habitat
Colon and cecum

Pathogenic stage
Trophozoite

Locomotive apparatus
Pseudopodia ("false foot”")

Motility
Active, progressive and directional

Nucleus
'Ring and dot' appearance: peripheral chromatin and central karyosome

Mode of reproduction
Binary fission

Pathogenesis
Lytic necrosis (it looks like “flask-shaped” holes in Gastrointestinal tract sections (GIT)

Type of encystment
Protective and Reproductive

Lab diagnosis
Most common is direct fecal smear (DFS) and staining (but does not allow identification to species level); enzyme immunoassay (EIA); indirect hemagglutination (IHA); Antigen detection – monoclonal antibody; PCR for species identification. Sometimes only the use of a fixative (formalin) is effective in detecting cysts. Culture: From faecal samples - Robinson's medium, Jones' medium

Treatment
Metronidazole for the invasive trophozoites PLUS a lumenal amoebicide for those still in the intestine. Paromomycin (Humatin) is the luminal drug of choice, since Diloxanide furoate (Furamide) is not commercially available in the USA or Canada (being available only from the Centers for Disease Control and Prevention). A direct comparison of efficacy showed that Paromomycin had a higher cure rate.[23] Paromomycin (Humatin) should be used with caution in patients with colitis, as it is both nephrotoxic and ototoxic. Absorption through the damaged wall of the intestinal tract can result in permanent hearing loss and kidney damage. Recommended dosage: metronidazole 750 mg three times a day orally, for 5 to 10 days followed by paromomycin 30 mg/kg/day orally in 3 equal doses for 5 to 10 days or Diloxanide furoate 500 mg 3 times a day orally for 10 days, to eradicate lumenal amoebae and prevent relapse.[24][25]

Trophozoite stage

Pathognomonic/diagnostic feature
Ingested RBC; distinctive nucleus

Cyst Stage

Chromatoidal body
'Cigar' shaped bodies (made up of crystalline ribosomes)

Number of nuclei
1 in early stages, 4 when mature

Pathognomonic/diagnostic feature
'Ring and dot' nucleus and chromatoid bodies

text: Meiosis[edit]

text: In sexually reproducing eukaryotes, homologous recombination (HR) ordinarily occurs during meiosis. The meiosis-specific recombinase, Dmc1, is required for efficient meiotic HR, and Dmc1 is expressed in E. histolytica.[26] The purified Dmc1 from E. histolytica forms presynaptic filaments and catalyzes ATP-dependent homologous DNA pairing and DNA strand exchange over at least several thousand base pairs.[26] The DNA pairing and strand exchange reactions are enhanced by the eukaryotic meiosis-specific recombination accessory factor (heterodimer) Hop2-Mnd1.[26] These processes are central to meiotic recombination, suggesting that E. histolytica undergoes meiosis.[26]

text: Several other genes involved in both mitotic and meiotic HR are also present in E. histolytica.[27] HR is enhanced under stressful growth conditions (serum starvation) concomitant with the up-regulation of HR-related genes.[28] Also, UV irradiation induces DNA damage in E. histolytica trophozoites and activates the recombinational DNA repair pathway.[27] In particular, expression of the Rad51 protein (a recombinase) is increased about 15-fold by UV treatment.