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Print-Friendly"Immune" to HIV? Not So Fast
March 7, 2012
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As has been reported for a few years, people with a delta 32/delta 32 mutation of the gene that governs the CCR5 receptor are resistant to HIV infection -- at least from viruses using the CCR5 receptor. A group of researchers from the Autonomous University of Barcelona has been able to identify one of these individuals who has actually been infected with CXCR4-tropic virus. We all suspected this could happen, but this is the first case report of such a person.
It is believed that people infected with X4-tropic HIV do not fare as well as those infected with R5-tropic virus. However, this individual is doing well despite having been infected in 1996.
The research team believes that the individual's good viral control on HAART has to do with the presence of HLA-B*5701. HLA-B (major histocompatibility complex, class I, B) is a human gene that provides instructions for making a protein that plays a critical role in the immune system. It is part of a family of genes called the human leukocyte antigen (HLA) complex. The HLA complex helps the immune system distinguish the body's own proteins from proteins made by foreign invaders such as viruses and bacteria.
The HLA-B gene has many different normal variations, allowing each person's immune system to react to a wide range of foreign invaders. Hundreds of versions (alleles) of HLA-B are known, each of which is given a particular number.
A version of HLA-B designated HLA-B*5701 is associated with slower HIV disease progression and extreme sensitivity to abacavir (ABC, Ziagen). People with abacavir hypersensitivity often develop a fever, chills, rash, upset stomach, and other symptoms when treated with this drug.
This poster reinforces what we have been telling Timothy Brown (the Berlin patient): Even if you are "immune" to CCR5-tropic HIV, you still need to protect yourself against X4-tropic virus infection. X4-tropic virus infection in patients with the double delta 32 mutation in their CCR5 gene does not seem very common but, as described in this case report, it is possible. And patients like Brown are vulnerable to it.
For more information, read CROI poster 292, "HIV-1 Infection in a CCR5-D32/D32, HLA-B*5701, and HLA-A*2402 Subject: A Case Report," presented by Ester Ballana.
This article was provided by TheBodyPRO.com. It is a part of the publication The 19th Conference on Retroviruses and Opportunistic Infections.|
Reader Comments:
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Unfortunately, they didn't report the mode of infection since sexual transmission of X4 virus is very uncommon.
To find out if you ment the so called Hiv1 and Hiv2 virus, i clicked on the link and saw that the link only was ment for people at the now ongoing conference, i am a long time survivor Tested HIV+ in spring '89 and chronic carrier of Hep.B since 1980 and developed extreme rash when taking Abacavir and switched to Isentress on advice/suggestion Body.com and Truvada, Abacavir was earlier replaced by Norvir and Reyataz but after being on trial version(Norvir and Saquinavir in the 90's my third and last trial)i developed extreme diahrea and needed Truvada for its sideeffect against the Hep.B virus. Did used for years 3TC on trial basis. My Question comment is by which variant of the Hiv virus could Tim..B.ow. get killed ? cause he got stamcells twice from someone immune for the Hiv1 virus. Know that dark people with the Hiv2 virus have less treatmentoptions. Second comment is it possible that a Hiv3 virus can develop cause original all Hivvirusses have the Sivvirus from chimps in common. And why/when did the split up go in the the 2 hivvirusses. Greetings Joost
"this is the first case report...." - I respectfully point out that this statement is incorrect, as there have been multiple reports of HIV infection of people who are homozygous for CCR5 delta 32, as early as 1997 (Biti et al. Nat. Med.; O'Brien et al. Lancet; Theodorou et al. Lancet). The latter 2 reports characterized the gp120 sequences in those individuals as characteristic of the "syncytium-inducing" phenotype, which is typically associated with CXCR4 use. Subsequently multiple cases of HIV infection despite CCR5 delta32 homozygosity have been reported, typically involving CXCR4-using viruses.
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| Please note: Knowledge about HIV changes rapidly. Note the date of this summary's publication, and before treating patients or employing any therapies described in these materials, verify all information independently. If you are a patient, please consult a doctor or other medical professional before acting on any of the information presented in this summary. For a complete listing of our most recent conference coverage, click here. |
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