Chronic HIV-1 Infection Frequently Fails To Protect Against Superinfection
Main Category: HIV / AIDSArticle Date: 15 Nov 2007 - 17:00 PDT
Natural HIV-1 infection does not always elicit a protective immune response, according to a new study published November 16 in PLoS Pathogens. The team of researchers from Washington University, the Fred Hutchinson Cancer Research Center of Seattle, and the University of Nairobi show how HIV-1 vaccines may not be as reliable against superinfection as once thought.
Superinfection of HIV-1 occurs when an individual infected with one strain of HIV-1 acquires a second strain. Currently there are over 20 published cases of HIV-1 superinfection, most of which have been focused on individuals who have been carefully monitored during their infection. These cases prove that an HIV-1 vaccine may not always protect against infection by a different strain. But because there have been reports of selected individuals, it has been unclear how commonly HIV-1 re-infection occurs.
To address this question, Dr. Julie Overbaugh and her research team investigated the incidence of HIV-1 superinfection in 36 high-risk women followed roughly five years after their initial infection.
Seven cases of superinfection were found; five of them occurring over a year past initial infection. Additionally, three of the seven cases displayed a virus from the same HIV-1 genetic subtype.
This study suggests that immune responses found in natural HIV-1 infection, which fail to provide protection against re-infection, may not be the best path to an effective HIV-1 vaccine.
CITATION: Piantadosi A, Chohan B, Chohan V, McClelland RS, Overbaugh J (2007) Chronic HIV-1 infection frequently fails to protect against superinfection. PLoS Pathog 3(11):e177. doi:10.1371/journal.ppat.0030177 Please click here.
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Adjuvant Infections As An Explanation For Lack Of Effectivity Of Vaccines
posted by Cristina Grassi on 14 Dec 2007 at 10:19 amIn a paper that was published in 2001 (see reference at the end of this commentary), we propose that HIV productive infections of CD4+ T cells occur mainly on activated cells and although the virus can infect both, resting and activated cells, productive infections occur mainly in the latter than in the former. In this paper we conclude that the technological development of vaccines should be focused to a highly controlled and specific immune reaction.
Similarly, immunotherapeutics could focus towards avoiding immune activation. The rational takes into account the role of all the agents that promote cell activation (including vaccination) thus increasing productive infections. This effect was named as "adjuvant activation" or "adjuvant effect" and is consistent with the idea that any immune challenge of an HIV infected person will promote the opportunities for productive infections.
Conversely, the infection with HIV of a healthy vaccinated person, will encounter a highly activatable cell polulation, if the vaccine is not properly designed. This proposal is in agreement with the findings reported in "Chronic HIV-1 Infection Frequently Fails To Protect Against Superinfection" as well as with other findings such as in "STATEMENT Immunizations Are Discontinued in Two HIV Vaccine Trials" (NIH News). Finally, it is important to say that the adjuvant activation is a plausible explanation for the natural history of the development of the AIDS epidemic from the standpoint of an emerging infection due to the increased risk caused by anthropogenic activities, and it also considers the progression of the infection to the syndrome, in terms of cellular population dynamics.
H. C. Grassi, E. D. J. Andrade. HIV infections and AIDS development: the role of adjuvant activation.Medical Hypotheses (2001) 57(6), 693-696.
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