Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America
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.
Risk of transmission from infected health care practitioners who take appropriate precautions unclear but appears minimal. In the 1980s, one dentist transmitted HIV to ≥ 6 of his patients by unknown means. However, extensive investigations of patients cared for by other HIV-infected physicians, including surgeons, have uncovered few other cases.
Jump up ^ Holmes CB, Losina E, Walensky RP, Yazdanpanah Y, Freedberg KA (2003). “Review of human immunodeficiency virus type 1-related opportunistic infections in sub-Saharan Africa”. Clin. Infect. Dis. 36 (5): 656–662. doi:10.1086/367655. PMID 12594648.
The typical course of an infection with HIV is illustrated in Fig. 11.21. However, it has become increasingly clear that the course of the disease can vary widely. Thus, although most people infected with HIV go on to develop AIDS and ultimately to die of opportunistic infection or cancer, this is not true of all individuals. A small percentage of people seroconvert, making antibodies against many HIV proteins, but do not seem to have progressive disease, in that their CD4 T-cell counts and other measures of immune competence are maintained. These long-term nonprogressors have unusually low levels of circulating virus and are being studied intensively to determine how they are able to control their HIV infection. A second group consists of seronegative people who have been highly exposed to HIV yet remain disease-free and virus-negative. Some of these people have specific cytotoxic lymphocytes and TH1 lymphocytes directed against infected cells, which confirms that they have been exposed to HIV or possibly noninfectious HIV antigens. It is not clear whether this immune response accounts for clearing the infection, but it is a focus of considerable interest for the development and design of vaccines, which we will discuss later. There is a small group of people who are resistant to HIV infection because they carry mutations in a cell-surface receptor that is used as a co-receptor for viral entry, as we will see below.
^ Jump up to: a b Morgan D, Mahe C, Mayanja B, Okongo JM, Lubega R, Whitworth JA (2002). “HIV-1 infection in rural Africa: is there a difference in median time to AIDS and survival compared with that in industrialized countries?”. AIDS. 16 (4): 597–632. doi:10.1097/00002030-200203080-00011. PMID 11873003.
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.
How would it make u feel, if someone u knew had aids? Would u feel sad or sorry for them or treat them as the living breatheing human that they are, with or without tne diease. Would you stop to think how scared they were or just judge them? People assume there is only one way to get aids and that is by being gay. Our world is VERY NARROW MINDED. Imagine how u would feel, and how u wouldn’t want someone to stop loving you as a PERSON, just because u contracted it. Hospital needles not properly disposed of, that one may get pricked with. If u have to have a transfusion. Passing it thru sex, comes when u didn’t realize u had contracted it some how. I know someone, whom I dearly love with this hidden demon, I see his sadness and feel his pain, “for if anyone knew…… they would change how they really looked at him. We all are going to die, each of us in different ways….. so we should live, love and not stereo type while we are alive. I have learned alot just by knowing this person and u know what? I enjoy every minute and every conversation, every laugh and smile, because i know it makes a difference in their world too! Get educated and open ur mind and ur heart to everyone.
In individuals not infected with HIV, the CD4 count in the blood is normally above 400 cells per mm3 of blood. People generally do not become at risk for HIV-specific complications until their CD4 cells are fewer than 200 cells per mm3. At this level of CD4 cells, the immune system does not function adequately and is considered severely suppressed. A declining number of CD4 cells means that HIV disease is advancing. Thus, a low CD4 cell count signals that the person is at risk for one of the many opportunistic infections that occur in individuals who are immunosuppressed. In addition, the actual CD4 cell count indicates which specific therapies should be initiated to prevent those infections.
Studies with powerful drugs that completely block the cycle of HIV replication indicate that the virus is replicating rapidly at all phases of infection, including the asymptomatic phase. Two viral proteins in particular have been the target of drugs aimed at arresting viral replication. These are the viral reverse transcriptase, which is required for synthesis of the provirus, and the viral protease, which cleaves the viral polyproteins to produce the virion proteins and viral enzymes. Inhibitors of these enzymes prevent the establishment of further infection in uninfected cells. Cells that are already infected can continue to produce virions because, once the provirus is established, reverse transcriptase is not needed to make new virus particles, while the viral protease acts at a very late maturation step of the virus, and inhibition of the protease does not prevent virus from being released. However, in both cases, the released virions are not infectious and further cycles of infection and replication are prevented.
If you’ve been exposed to HIV, but test negative during the window, you might benefit from pre-exposure prophylaxis (PrEP). A combination of HIV-approved drugs, PrEP can lower the risk of contracting or spreading HIV when taken consistently.
If the CD4 count drops below 50 cells per microliter of blood, azithromycin taken weekly or clarithromycin taken daily may prevent Mycobacterium avium complex infections. If people cannot take either of these drugs, they are given rifabutin.
For people who are taking antiretrovirals and are rigidly compliant, this phase can be interrupted, with complete viral suppression. Effective antiretrovirals arrest on-going damage to the immune system.
Puhan MA, Van Natta ML, Palella FJ, Addessi A, Meinert C. Excess mortality in patients with AIDS in the era of highly active antiretroviral therapy: temporal changes and risk factors. Clin Infect Dis. 2010 Oct 15. 51(8):947-56. [Medline]. [Full Text].
It is known that normal cell cycling is necessary to produce a normal cytokine profile  and that HIV causes cell-cycle arrest.  Whether this is the exact mechanism is unresolved, however. Analysis of cytokine levels in HIV infected, uninfected, and HAART-treated patients with HIV show that cytokines involved in T-cell homeostasis were definitely affected, and therapy partially corrected these defects. In particular there was decreased IL-7, IL-12, IL-15 and FGF-2, and increased TNF-alpha and IP-10. [42, 43]
Within 2 to 4 weeks after infection with HIV, people may experience a flu-like illness, which may last for a few weeks. This is the body’s natural response to infection. When people have acute HIV infection, they have a large amount of virus in their blood and are very contagious. But people with acute infection are often unaware that they’re infected because they may not feel sick right away or at all. To know whether someone has acute infection, either a fourth-generation antibody/antigen test or a nucleic acid (NAT) test is necessary. If you think you have been exposed to HIV through sex or drug use and you have flu-like symptoms, seek medical care and ask for a test to diagnose acute infection.
Jump up ^ McGovern SL, Caselli E, Grigorieff N, Shoichet BK (2002). “A common mechanism underlying promiscuous inhibitors from virtual and high-throughput screening”. Journal of Medicinal Chemistry. 45 (8): 1712–22. doi:10.1021/jm010533y. PMID 11931626.
Sexual practices such as fellatio and cunnilingus appear to be relatively low risk but not absolutely safe (see Table: HIV Transmission Risk for Several Sexual Activities). Risk does not increase significantly if semen or vaginal secretions are swallowed. However, open sores in the mouth may increase risk.
Pakker NG, Notermans DW, de Boer RJ, et al. Biphasic kinetics of peripheral blood T cells after triple combination therapy in HIV-1 infection: a composite of redistribution and proliferation. Nat Med. 1998 Feb. 4(2):208-14. [Medline]. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]