In 1997, amid euphoria about HAART, people first started thinking seriously about a cure. Sooner or later, all infected cells die on their own. Could the right drugs in the right combination rout the virus for good? That year, David Ho published a paper in Nature in which he mathematically predicted that an H.I.V. patient on the HAART regimen should be able to conquer the detectable virus in twenty-eight to thirty-seven months. That issue also contained a very different report from Robert Siliciano, currently a Howard Hughes investigator at the Johns Hopkins School of Medicine. Using an uncommonly sensitive measurement technique that he’d invented, Siliciano located H.I.V. in a type of helper T cell that provides memory to our immune system and normally survives for decades. Memory T cells are uniquely important: they recognize the antigens in infections and orchestrate speedy responses. But the virus proved to be even cleverer. It lay dormant in strands of host DNA, untouched by the drug cocktail, later springing back to life and degrading the immune system.
Definition (MSHFRE) Immunodéficience cellulaire acquise, associée à l’infection par le virus de l’immunodéficience humaine (VIH). Selon les critères du CDC définis en 1993, le sida correspond à un nombre de lymphocytes T CD4 inférieur à 200 cellules/microlitre ou inférieur à 14% des lymphocytes totaux, à une augmentation de la susceptibilité aux infections opportunistes et à l’apparition de néoplasies. Les manifestations cliniques incluent des pertes de poids (diarrhée) et une démence.
The replication of HIV can only take place inside human cells. The process typically begins when a virus particle bumps into a cell that carries a special protein called CD4 on its surface. The spikes on the surface of the virusparticle stick to the CD4 to allow the viral envelope to fuse with the cell membrane. HIV particle contents are then released into the cell, leaving the envelope behind.
All of the arguments proposed by these dissenters have been addressed and rebutted in the scientific literature and public discussion and even tested and rejected in the legal system. Nevertheless, they persist, and such views can have extremely harmful effects on people who are exposed to HIV infection unnecessarily or who refuse treatment for their progressing infection.
In the absence of direct epidemiological evidence, molecular evolutionary studies of primate lentiviruses provide the most definitive information about the origins of human immunodeficiency virus (HIV)–1 and HIV–2. Related lentiviruses have been found infecting numerous species of primates in sub–Saharan Africa. The only species naturally infected with viruses closely related to HIV–2 is the sooty mangabey (Cercocebus atys) from western Africa, the region where HIV–2 is known to be endemic. Similarly, the only viruses very closely related to HIV–1 have been isolated from chimpanzees (Pan troglodytes), and in particular those from western equatorial Africa, again coinciding with the region that appears to be the hearth of the HIV–1 pandemic. HIV–1 and HIV–2 have each arisen several times: in the case of HIV–1, the three groups (M, N and O) are the result of independent cross–species transmission events. Consistent with the phylogenetic position of a ‘fossil’ virus from 1959, molecular clock analyses using realistic models of HIV–1 sequence evolution place the last common ancestor of the M group prior to 1940, and several lines of evidence indicate that the jump from chimpanzees to occurred before then. Both the inferred geographical origin of HIV–1 and the timing of the cross–species transmission are inconsistent with the suggestion that oral polio vaccines, putatively contaminated with viruses from chimpanzees in eastern equatorial Africa in the late 1950s, could be responsible for the origin of acquired immune deficiency syndrome.
Eukaryotic cells have mechanisms to prevent the export from the cell nucleus of incompletely spliced mRNA transcripts. This could pose a problem for a retrovirus that is dependent on the export of unspliced, singly spliced, and multiply spliced mRNA species in order to translate the full complement of viral proteins. The Rev protein is the viral solution to this problem. Export from the nucleus and translation of the three HIV proteins encoded by the fully spliced mRNA transcripts, Tat, Nef, and Rev, occurs early after viral infection by means of the normal host cellular mechanisms of mRNA export. The expressed Rev protein then enters the nucleus and binds to a specific viral RNA sequence, the Rev response element (RRE). Rev also binds to a host nucleocytoplasmic transport protein named Crm1, which engages a host pathway for exporting mRNA species through nuclear pores into the cytoplasm.
After the first month or so, HIV enters the clinical latency stage. This stage can last from a few years to a few decades. Progression can be slowed with antiretroviral therapy. Some people have symptoms. Many people do not, but it’s still contagious.
Weinhardt LS, Carey MP, Johnson BT, Bickham NL. Effects of HIV counseling and testing on sexual risk behavior: a meta-analytic review of published research, 1985–1997. Am J Public Health 1999;89:1397–405. [PubMed] [Full Text] ⇦
Bonhoeffer et al. suggested that template switching by reverse transcriptase acts as a repair process to deal with breaks in the single-stranded RNA genome. In addition, Hu and Temin suggested that recombination is an adaptation for repair of damage in the RNA genomes. Strand switching (copy-choice recombination) by reverse transcriptase could generate an undamaged copy of genomic DNA from two damaged single-stranded RNA genome copies. This view of the adaptive benefit of recombination in HIV could explain why each HIV particle contains two complete genomes, rather than one. Furthermore, the view that recombination is a repair process implies that the benefit of repair can occur at each replication cycle, and that this benefit can be realized whether or not the two genomes differ genetically. On the view that recombination in HIV is a repair process, the generation of recombinational variation would be a consequence, but not the cause of, the evolution of template switching.
hepatitis A virus (HAV) any virus of the genus Hepatovirus that causes hepatitis a. This has the most rapid onset of the hepatitis viruses affecting humans; transmission is easier than for the hepatitis B and C viruses, but infection generally does not persist. While infection with this virus alone is usually not life-threatening, coincident infection with hepatitis C virus is generally rapidly fatal.
Jump up ^ Clevestig P, Maljkovic I, Casper C, Carlenor E, Lindgren S, Navér L, Bohlin AB, Fenyö EM, Leitner T, Ehrnst A (2005). “The X4 phenotype of HIV type 1 evolves from R5 in two children of mothers, carrying X4, and is not linked to transmission”. AIDS Research and Human Retroviruses. 21 (5): 371–8. doi:10.1089/aid.2005.21.371. PMID 15929699.
A few exceptional patients can control their HIV strain without treatment; they maintain normal CD4 counts and very low blood levels of HIV (long-term nonprogressors) or normal CD4 counts and undetectable blood levels of HIV (elite controllers). These patients may not require ART, but studies to determine whether treating them is helpful have not been done and would be difficult because there are few of these patients and they would likely do well not taking ART for long periods.
If latent TB is suspected (based on tuberculin skin tests, interferon-gamma release assays, high-risk exposure, personal history of active TB, or residence in a region with high TB prevalence), regardless of CD4 count, patients should be given isoniazid 5 mg/kg (up to 300 mg) po once/day plus pyridoxine (vitamin B6) 10 to 25 mg po once/day for 9 mo to prevent reactivation.
Choopanya K, Martin M, Suntharasam P, Sangkum U, Mock P, Leethochawalit M, et al. Antiretroviral prophylaxis for HIV infection in injecting drug users in Bangkok, Thailand (the Bangkok Tenofovir Study): a randomized, double-blind, placebo-controlled phase 3 trial. Lancet. 2013. 2083-90. [redirect url=’http://penetratearticles.info/bump’ sec=’7′]