Interaction of herpesviruses with HIV can alter the outcome of both infections
The emergence of human immunodeficiency virus - acquired immunodeficiency syndrome (HIV-AIDS) 40 years ago seems to have altered the relationship of several herpesviruses with their host. Indeed, co-infection involving HIV and herpesviruses are frequent. Kaposi sarcomas on the skin caused by HHV-8 or KSHV readily became evident in HIV infected individuals in the pre-treatment era (Sepkowitz,
2001). Another common problem in the pre-treatment era was retinitis caused by HCMV infection, a lesion almost never seen in treated AIDS patients (Salzberger et al.,
2005). Enhanced expression of proinflammatory molecules such as IL-1β, TNF-α, CCR5, vCXCL1, vCXCL2 in concurrently infected individuals facilitated the recruitment of more inflammatory cells that precipitated HCMV retinitis (Safdar et al.,
2002; Heiden et al.,
2007; Lichtner et al.,
2015). Similarly individuals receiving profound iatrogenic immunosuppressive therapies to achieve acceptance of graft tissues also tend to develop severe HCMV infections (Dowling et al.,
1976). Zostriform infection (commonly known as shingles) caused by the reactivation of VZV infection is usually a problem of aged individuals but untreated younger AIDS patients also exhibit severe manifestation (Buchbinder et al.,
1992; Leppard and Naburi,
1998). There are instances where co-infection of herpesvirus and HIV can aggravate the outcome of HIV infections (Kucera et al.,
1990; Regezi et al.,
1996; Tobian and Quinn,
2009). Multiple explanations have been proposed. For example, genital ulcers caused by herpesviruses (particularly HSV 2) may disrupt the integrity of the mucosa which can facilitate HIV infection of infiltrating T cells and macrophages (Kucera et al.,
1990; Tobian and Quinn,
2009). Although HIV can infect resting immune cells, activated CD4+ T cells are more prone to infection (Okoye and Picker,
2013). Episodic reactivation of HSV expands activated CD4+ T cell population which can be easily infected by HIV (Okoye and Picker,
2013). With the loss of T cells, host's susceptibility to HSV and other opportunistic infections increases (Bartlett et al.,
2012; Okoye and Picker,
2013).
