The interval from HIV infection to diagnosis has decreased in recent years, but diagnosis delays continue to be substantial for some population segments. Whereas testing in the past 12 months has increased in recent years among groups at high risk, a high proportion of persons in all risk groups remain untested, with many missed opportunities for testing. Diagnosis delays lead to missed opportunities for HIV care and treatment and prolong the time a person is unaware of their infection, increasing the potential for HIV transmission. For care and treatment to reduce HIV incidence effectively, a high proportion of cases need to be diagnosed and treated soon after infection occurs. Continued efforts to determine why cases are not being diagnosed soon after infection and to assure implementation of routine and targeted testing can help reduce both the number of persons unaware of their infection and diagnosis delays.
A safe and effective vaccine for the prevention of HIV infection and AIDS is an attractive goal, but its achievement is fraught with difficulties that have not been faced in developing vaccines against other diseases. The first problem is the nature of the infection itself, featuring a virus that proliferates extremely rapidly and causes sustained infection in the face of strong cytotoxic T-cell and antibody responses. As we discussed in Section 11-25, HIV evolves in individual patients by the selective proliferative advantage of mutant virions encoding peptide sequence changes that escape recognition by antibodies and by cytotoxic T lymphocytes. This evolution means that the development of therapeutic vaccination strategies to block the development of AIDS in HIV-infected patients will be extremely difficult. Even after the viremia has been largely cleared by drug therapy, immune responses to HIV fail to prevent drug-resistant virus from rebounding and replicating at pretreatment levels.
Jump up ^ Woods, S.; Moore, D.; Weber, E.; Grant, I. (2009). “Cognitive neuropsychology of HIV-associated neurocognitive disorders”. Neuropsychology review. 19 (2): 152–168. doi:10.1007/s11065-009-9102-5. PMC 2690857 . PMID 19462243.
Clinical findings Weight loss exceeding 10% of body weight, protracted asthenia, continuous fever for >1 month, diarrhoea >1 month, persistent cough, oropharyngeal candidiasis, relapsing cutaneous herpes, generalised pruritic dermatosis, generalised lymphadenopathy, Kaposi’s sarcoma.
Jump up ^ Choopanya, Kachit; Martin, Michael; Suntharasamai, Pravan; Sangkum, Udomsak; Mock, Philip A; Leethochawalit, Manoj; Chiamwongpaet, Sithisat; Kitisin, Praphan; Natrujirote, Pitinan; Kittimunkong, Somyot; Chuachoowong, Rutt; Gvetadze, Roman J; McNicholl, Janet M; Paxton, Lynn A; Curlin, Marcel E; Hendrix, Craig W; Vanichseni, Suphak (June 1, 2013). “Antiretroviral prophylaxis for HIV infection in injecting drug users in Bangkok, Thailand (the Bangkok Tenofovir Study): a randomised, double-blind, placebo-controlled phase 3 trial”. The Lancet. 381 (9883): 2083–2090. doi:10.1016/S0140-6736(13)61127-7. PMID 23769234.
Human immunodeficiency virus (HIV) is a blood-borne, sexually transmissible virus (see the image below.) The virus is typically transmitted via sexual intercourse, shared intravenous drug paraphernalia, and mother-to-child transmission (MTCT), which can occur during the birth process or during breastfeeding.
Gut-associated lymphoid tissue (GALT) plays a role in HIV replication.  Although the portal of entry for HIV infection is typically through direct blood inoculation or exposure of the virus to genital mucosal surfaces, the GI tract contains a large amount of lymphoid tissue, making this an ideal site for HIV replication.
Jump up ^ Huang, L; Cattamanchi, A; Davis, JL; den Boon, S; Kovacs, J; Meshnick, S; Miller, RF; Walzer, PD; Worodria, W; Masur, H; International HIV-associated Opportunistic Pneumonias (IHOP), Study; Lung HIV, Study (June 2011). “HIV-associated Pneumocystis pneumonia”. Proceedings of the American Thoracic Society. 8 (3): 294–300. doi:10.1513/pats.201009-062WR. PMC 3132788 . PMID 21653531.
HIV replicates in activated T cells (its promotor contains a nuclear factor kappa B [NF-kappa-B]–binding region, the same protein that promotes other proteins in activated T cells and macrophages), and activated T cells migrate to the lymph nodes. As such, much of the viral replication occurs outside of the peripheral blood, even though serum viral load is still a useful surrogate marker of viral replication.
Immunodeficiency disorders are either congenital or acquired. A congenital, or primary, disorder is one you were born with. Acquired, or secondary, disorders you get later in life. Acquired disorders are more common than congenital disorders.
HIV-1 is the most common and pathogenic strain of the virus. Scientists divide HIV-1 into a major group (Group M) and two or more minor groups, namely Group N, O and possibly a group P. Each group is believed to represent an independent transmission of SIV into humans (but subtypes within a group are not). A total of 39 ORFs are found in all six possible reading frames (RFs) of HIV-1 complete genome sequence, but only a few of them are functional.
Newer point-of-care tests using blood or saliva (eg, particle agglutination, immunoconcentration, immunochromatography) can be done quickly (in 15 min) and simply, allowing testing in a variety of settings and immediate reporting to patients. Positive results of these rapid tests should be confirmed by standard blood tests (eg, ELISA with or without Western blot) in developed countries and repetition with one or more other rapid tests in developing countries. Negative tests need not be confirmed.
Jump up ^ Horvath, T; Madi, BC; Iuppa, IM; Kennedy, GE; Rutherford, G; Read, JS (January 21, 2009). Horvath, Tara, ed. “Interventions for preventing late postnatal mother-to-child transmission of HIV”. Cochrane Database of Systematic Reviews (1): CD006734. doi:10.1002/14651858.CD006734.pub2. PMID 19160297.
Administration of HIV treatment to HIV-positive pregnant women during pregnancy and labour and after delivery, as well as to the newborn baby, dramatically reduces the risk of mother-to-baby transmission of HIV.
Over time, HIV can destroy so many of these cells that the body can’t fight off infections and disease. These opportunistic infections or cancers take advantage of a very weak immune system and signal that the person has AIDS, the last stage of HIV infection….Read more about HIV/AIDS
Jump up ^ Kuhar DT, Henderson DK, Struble KA, et al. (September 2013). “Updated US Public Health Service Guidelines for the Management of Occupational Exposures to Human Immunodeficiency Virus and Recommendations for Postexposure Prophylaxis”. Infect Control Hosp Epidemiol. 34 (9): 875–92. doi:10.1086/672271. PMID 23917901.
In August, Janet and Robert Siliciano wrote about the Brigham men and the Mississippi baby in Science, saying that the cases confirmed that researchers were on the right path in attacking latent infection. The Berlin patient was an even more compelling example. Karl Salzwedel, the chief of Pathogenesis and Basic Research in the Division aids at the National Institute of Allergy and Infectious Diseases, told me that until Timothy Brown “it wasn’t really clear how we would go about getting rid of the last bits of virus that remain in the reservoir.” Brown’s case provided “a proof of concept: it may be possible to eradicate latent H.I.V. from the body. It may be from a very risky and toxic method, but it’s proof of concept nonetheless.”
Since the discovery of HIV and its link to AIDS, great strides have been made in understanding its biology and in developing effective treatments. The difficulty in dealing with HIV on a global scale is largely due to the fact that HIV infection is far more common in resource-poor countries.
Lennox JL, DeJesus E, Lazzarin A, et al. Safety and efficacy of raltegravir-based versus efavirenz-based combination therapy in treatment-naive patients with HIV-1 infection: a multicentre, double-blind randomised controlled trial. Lancet. 2009 Sep 5. 374(9692):796-806. [Medline].
Successfully treated patients may demonstrate intermittent low-level viremia (eg, < 400 copies/mL), but this is not thought to represent viral replication or to predict virologic failure (defined as a confirmed viral load of > 200 copies/mL 
Acronym for acquired immune deficiency (or immunodeficiency) syndrome; disorder of the immune system characterized by opportunistic diseases, including candidiasis, Pneumocystis jiroveci pneumonia, oral hairy leukoplakia, herpes zoster, Kaposi sarcoma, toxoplasmosis, isosporiasis, cryptococcosis, non-Hodgkin lymphoma, and tuberculosis. The syndrome is caused by the human immunodeficiency virus (HIV-1, groups M and O, and HIV-2), which is transmitted in body fluids (notably breast milk, blood, and semen) through sexual contact, sharing of contaminated needles (by IV drug abusers), accidental needle sticks, contact with contaminated blood, or transfusion of contaminated blood or blood products. Hallmark of the immunodeficiency is depletion of T4+ or CD4+ helper/inducer lymphocytes, primarily the result of selective tropism of the virus for the lymphocytes.
HIV/AIDS; retrovirusScanning electron micrograph of HIV-1 virions (green) budding from a cultured lymphocyte. Multiple round bumps on the cell surface represent sites of virion assembly and budding.C. Goldsmith/Centers for Disease Control and Prevention (CDC) [redirect url=’http://penetratearticles.info/bump’ sec=’7′]