Acquired Immunodeficiency Syndrome: Müller-Trutwin M

Hurtrel B, Petit F, Arnoult D, Müller-Trutwin M, Silvestri G, Estaquier J. · Unité de Physiopathologie des Infections Lentivirales, Institut Pasteur, Paris, cedex 15, France. · Cell Death Differ. · Pubmed #15818408 links to  free full text

Abstract: Pathogenic human immunodeficiency virus (HIV)/Simian immunodeficiency virus (SIV) infection is associated with increased T-cell apoptosis. In marked contrast to HIV infection in humans and SIV infection in macaques, the SIV infection of natural host species is typically nonpathogenic despite high levels of viral replication. In these nonpathogenic primate models, no observation of T-cell apoptosis was observed, suggesting that either SIV is less capable of directly inducing apoptosis in natural hosts (likely as a result of coevolution/coadaptation with the host) or, alternatively, that the indirect T-cell apoptosis plays the key role in determining the HIV-associated T-cell depletion and progression to acquired immune deficiency syndrome (AIDS). Understanding the molecular and cellular mechanisms responsible for the disease-free equilibrium in natural hosts for SIV infection, including those determining the absence of high levels of T-cell apoptosis, is likely to provide important clues regarding the mechanisms of AIDS pathogenesis in humans.

Courgnaud V, Müller-Trutwin M, Sonigo P. · Laboratoire des rétrovirus UR 36, 911, avenue Agropolis, BP 64501, 34034 Montpellier Cedex 5, France. · Med Sci (Paris). · Pubmed #15124118 links to  free full text

Abstract: While the AIDS epidemic caused by human immunodeficiency viruses (HIV) has resulted in the death of over 20 million people worldwide, simian immunodeficiency virus (SIV) infection, found in numerous African primate species, does not induce disease symptoms. The factors accounting for this difference between humans and natural host of SIV remain poorly understood. The entangled nature of the host/virus relationship could be the answer, rather than independent virus or host factors. Such a relationship is as a consequence of host/virus adaptation which has evolved over long periods in naturally infected primate species.

Pandrea I, Onanga R, Kornfeld C, Rouquet P, Bourry O, Clifford S, Telfer PT, Abernethy K, White LT, Ngari P, Müller-Trutwin M, Roques P, Marx PA, Simon F, Apetrei C. · Laboratoire de Virologie, UGENET, SEGC, Réserve de la Lopé, Centre de Primatologie, Centre International de Recherches Médicales, BP769, Franceville, Gabon, France. · Virology. · Pubmed #14675630 No free full text.

Abstract: Viral loads were investigated in SIVmnd-1 chronically infected mandrills and the results were compared with those previously observed in other nonpathogenic natural SIV infections. Four naturally and 11 experimentally SIVmnd-1-infected mandrills from a semi-free-ranging colony were studied during the chronic phase of infection. Four SIVmnd-1-infected wild mandrills were also included for comparison. Twelve uninfected mandrills were used as controls. Viral loads in all chronically infected mandrills ranged from 10(5) to 9 x 10(5) copies/ml and antibody titers ranged from 200 to 14,400 and 200 to 12,800 for anti-V3 and anti-gp36, respectively. There were no differences between groups of wild and captive mandrills. Both parameters were stable during the follow-up, and no clinical signs of immune suppression were observed. Chronic SIVmnd-1-infected mandrills presented slight increases in CD20+ and CD28+/CD8+ cell counts, and a slight decrease in CD4+/CD3+ cell counts. A slight CD4+/CD3+ cell depletion was also observed in old uninfected controls. Similar to other nonpathogenic models of lentiviral infection, these results show a persistent high level of SIVmnd-1 replication during chronic infection of mandrills, with minimal effects on T cell subpopulations.

Bégaud E, Feindirongai G, Versmisse P, Ipero J, Léal J, Germani Y, Morvan J, Fleury H, Müller-Trutwin M, Barré-Sinoussi F, Pancino G. · Institute Pasteur, Bangui, Central Africa Republic. · AIDS Res Hum Retroviruses. · Pubmed #12908932 No free full text.

Abstract: To study the progression of HIV-1 infection and coreceptor usages in Central African Republic, clinical data, plasma viral load, and coreceptor usage of sequential HIV-1 isolates were analyzed in a seroincident prospective cohort (PRIMOCA). Twenty-three HIV-1 infected individuals from the Central African Armed Forces were followed from 1995 to 2000. Viruses were isolated from 17 patients at various time points after seroconversion and their coreceptor usage was examined using GHOST cells expressing CD4 and one of the HIV-1 chemokine coreceptors CCR5, CXCR4, BOB/GPR15, and Bonzo/STRL33/CXCR6. Eleven patients died from AIDS. Eight of them died between 2 and 5 years after seroconversion, after a brief symptomatic stage. Patients who rapidly progressed to AIDS and death displayed the highest viral loads after seroconversion. All isolates obtained soon after seroconversion used CCR5, albeit, in some cases, CXCR4, BOB, or Bonzo were also used. Most isolates remained R5 (59 out of 61 isolates), although viruses using CXCR4 appeared in some cases of progression to AIDS. In several cases, a broad tropism was observed during the course of infection, with a frequent usage of BOB and Bonzo in addition to CCR5. Rapid progression to disease and short survival time among Central African HIV-1 patients appear more frequent than those reported in industrialized countries. Viral coreceptor used was mainly CCR5, but, interestingly, a large part of isolates also used BOB and Bonzo. However, there was no strict correlation between the clinical outcome and extended viral tropism.

Vergne L, Müller-Trutwin M, Lal RB, Tibayrenc M. · Laboratoire "Prise en charge du SIDA en Afrique", UR36, IRD, 911 Avenue Agropolis, BP 64501, 34394 Montpellier Cédex 5, France. · Infect Genet Evol. · Pubmed #12798012 No free full text.

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