[Frontiers in Bioscience 1, e42-54, August 1,1996]


Catherine Brenner, Olivier Neyrolles, Alain Blanchard

Institut Pasteur, Unité d'Oncologie Virale, Département SIDA et Rétrovirus, 28, rue du Dr. Roux, 75724 Paris Cedex 15, France

Received 07/05/96; Accepted 07/09/96; On-line 08/01/96


HIV-infection is associated with chronic but not maximal activation of the immune system (for review see 1). The persistence of virus replication throughout the course of HIV disease may contribute to the maintenance of this state of immune activation. Indeed activation is directly linked to the rate of HIV replication because retroviral infection of new cells is facilitated by cellular activation and also HIV replication is initiated in cells latently infected with the virus by cell activation. There is now considerable evidence that the quantity of virus in plasma is predictive of the evolution of the disease (2).

HIV-1 replication in vitro is facilitated by T cell activation and therefore by several co-infectious agents, including mycobacteria, Salmonella spp. (3), Leishmania donovani (4). However, little is known about the ability of antigenic stimulation to augment HIV-1 replication in vivo. Recent studies have shown that vaccination of HIV-1 infected individuals is followed by an transient increase of HIV replication (5-7). Therefore, an antigenic stimulation produced by infectious micro-organisms is likely to produce a similar increase in HIV replication that may last as long as the infection persists. Silent mycoplasmal infections could act in this way as HIV cofactors (8). This putative role of mycoplasmas (trivial names for members of the class Mollicute) in the evolution of HIV disease is not restrictive and they may also facilitate the transmission of HIV.

Indeed, numerous studies have established that ulcerative or non-ulcerative sexually transmitted diseases (STDs) favor homosexual and heterosexual HIV transmission (9-11). Urogenital mycoplasmas may thus facilitate local HIV acquisition. Although heterosexual transmission is currently the major mode of HIV infection worldwide, the contribution to the epidemic of the mother-to-child transmission is increasing, notably in Africa and South-East Asia. Vertical transmission is possible in utero and through breastfeeding, but is believed to be mostly during delivery. The mother's HIV infection stage (CD4+ cell count and viral load) is highly predictive of the probability of transmission. Other factors have also been implicated but to a lesser degree. In particular, sexually transmitted diseases (STDs) were proposed to increase the transmission of HIV during pregnancy and the treatment of these STDs may reduce vertical transmission (12). Urogenital mycoplasmas, in particular Ureaplasma urealyticum, are a common cause of chorioamnionitis and are vertically transmitted (13, 14). They may thus facilitate vertical HIV-transmission.

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