Herpes Simplex Virus Infection Induces Replication of Human Immunodeficiency Virus Type 1

Moriuchi, Masako; Moriuchi, Hiroyuki; Williams, Russell B.; Straus, Stephen E.

doi:10.1006/viro.2000.0667

Cited by 69 publications

(55 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…HSV-2 is believed to be the cause, not the effect, of increased HIV viral load, for several reasons. First, in vitro research shows that HSV gene products, such as infected cell protein (ICP)-0, ICP-4, ICP-27 and Us11, directly upregulate HIV replication (36)(37)(38)(39), and that HSV increases expression of HIV in infected macrophages through stimulation of the nuclear factor-kappa B pathway (40). The release of proinflammatory cytokines from HSV-infected cells could similarly stimulate HIV expression, as has been observed for other herpesviruses (41).…”

Section: Evidence That Hsv-2 Infection May Impact On Hiv Prognosismentioning

confidence: 98%

“…In support of this possibility, numerous in vitro experiments have shown that HSV-1 gene products can upregulate HIV expression, as mentioned above (36)(37)(38)(39)(40)60). Indeed, in contrast to the clinical literature on HSV-HIV coinfection, the majority of basic science literature on the molecular mechanisms of HSV-HIV interactions has focused on HSV-1, largely because of a greater availability of HSV-1 laboratory strains and animal models.…”

Section: Hsv-1 Is Similar To Hsv-2mentioning

confidence: 99%

See 1 more Smart Citation

Left out but not Forgotten: Should Closer Attention be Paid to Coinfection with Herpes Simplex Virus Type 1 and HIV?

Tan

Kaul

Walsmley

2009

Canadian Journal of Infectious Diseases and Medical Microbiolog

View full text Add to dashboard Cite

Herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) are among the most common coinfections seen in individuals infected with HIV-1. Most research on HSV-HIV coinfection has focused on HSV-2, and in particular, on its impact on HIV transmission. HSV-2 is associated with micro- and macroulcerations in genital mucosal surfaces, increased numbers of HIV target cells in genital mucosal tissue and increases in plasma HIV viral load of up to 0.5 log10copies/mL, such that HSV-2 infection increases the risk of both HIV acquisition and transmission. Because plasma HIV RNA levels are a major determinant of rates of CD4 cell decline, HSV-2 coinfection may also adversely affect the progression of HIV disease. Anti-HSV medications have in fact been associated with reciprocal decreases in HIV viral load in short-term studies. These findings have led to the development of several clinical trials of HSV-2 suppression as strategies for preventing HIV transmission and slowing the rate of HIV disease progression. HSV-1 coinfection has largely been ignored from this growing body of research, yet there are several reasons that this coinfection remains an important issue for study. First, the seroprevalence of HSV-1 is consistently higher than that of HSV-2 among both HIV-infected and HIV-uninfected populations, underscoring the relevance of HSV-1 coinfection to the majority of HIV-infected persons. Second, pre-existing HSV-1 antibodies in individuals may modulate the course of subsequently acquired HSV-2 infection; the implications of such changes on HSV-HIV coinfection remain unexplored. Third, HSV-1 and HSV-2 are closely related viruses that share 83% genetic homology. Their virological and pathobiological similarities suggest that their implications on HIV pathogenesis may be similar as well. Finally, HSV-1 is becoming increasingly relevant because the incidence of genital HSV-1 has risen. Although genital herpes is traditionally associated with HSV-2, recent studies have shown that the majority of serologically confirmed primary genital herpes in some settings is attributable to HSV-1. Because the genital tract is an important site of biological interaction between HSV and HIV, this epidemiological change may be clinically important.

show abstract

Section: Evidence That Hsv-2 Infection May Impact On Hiv Prognosismentioning

confidence: 98%

Section: Hsv-1 Is Similar To Hsv-2mentioning

confidence: 99%

Left out but not Forgotten: Should Closer Attention be Paid to Coinfection with Herpes Simplex Virus Type 1 and HIV?

Tan

Kaul

Walsmley

2009

Canadian Journal of Infectious Diseases and Medical Microbiolog

View full text Add to dashboard Cite

show abstract

“…Furthermore, infection with EBV may influence the expression of HIV because B cells transformed by EBV have the CD4 receptor to which HIV binds (Klatzmann et al 1984). More recently, studies have suggested that increased susceptibility to HIV by EBV infection may be related to greater expression of CCR5 on CD4 lymphocytes (Moriuchi and Moriuchi 2003;Moriuchi et al 2000;Tassan Din et al 2007). In addition, HIV has been shown to infect and multiply within B cells infected with EBV (Carbonari et al 1989).…”

Section: Stress and Acquisition Of Hivmentioning

confidence: 99%

“…Higher prevalence of drug use, incidence of ischemic heart disease, lower survival after myocardial infarction, heightened risk of hypertension, worse self-reported health, poorer physical functioning, higher number of chronic conditions and sexually transmitted diseases Boardman et al 2001;Brugal et al 2003;Chaix et al 2007;Cohen et al 2000;Cozier et al 2007;Das et al 2005;Espinoza et al 2007;Fleming et al 1997;Monteiro et al 2005;McQuillan et al 2004;Roca et al 1995 Glaser et al 1991;Glaser et al 1994;Herbert and Cohen 1993 Kiecolt- Glaser et al 2002 * ;Klatzmann et al 1984;Lin 1993;Margalith et al 1990;Moriuchi et al 2000;Moriuchi and Moriuchi 2003;Nerurkar et al 1987;Rahman et al 1991;…”

mentioning

confidence: 99%

Population Levels of Psychological Stress, Herpesvirus Reactivation and HIV

2008

View full text Add to dashboard Cite

Nearly 40,000 Americans are newly infected with Human Immunodeficiency Virus (HIV) each year. Recently, studies have demonstrated associations between group-level characteristics and the prevalence and incidence of HIV/Acquired Immune Deficiency Syndrome (AIDS) and other sexually transmitted diseases. Two mechanisms previously posited to explain these associations are neighborhood effects on risk behaviors and social or institutional policies. In this paper, we hypothesize that adversity at the population level, such as neighborhood poverty, also influences HIV risk through stress-mediated aberrations in immunological susceptibility by reviewing existing data examining each of these pathways. In particular, we review the evidence showing that: (1) Neighborhood ecologic stressors influence neighborhood-and individual-levels of mental health, psychosocial stress, and HIV/AIDS risk, (2) Individual-level psychosocial stressors influence progression from HIV to AIDS through stress-related hormonal changes, and (3) Individual-level psychosocial stressors influence HIV acquisition via stress-related reactivation of latent herpesviruses, specifically EBV and HSV-2. Our review indicates that further studies are needed to examine the joint pathways linking neighborhood-level sources of psychosocial stress, stress-related reactivation of HSV-2 and EBV, and increased acquisition rates of HIV. We suggest using a multi-level framework for targeting HIV prevention efforts that address not only behavioral risk factors, but structural, political, and institutional factors associated with neighborhood disadvantage, levels of psychosocial stress, and prevention or treatment of HSV-2 and EBV.

show abstract

“…HSV may potentiate HIV acquisition by disrupting or activating epithelial cells, which produce proinflammatory cytokines, and may activate or recruit HIV target cells. Additionally, heat-inactivated HSV particles enhance HIV replication in macrophages in vitro, by activating cellular pathways involving NF-B (24). HSV-infected epithelial cells may release noninfectious viral particles, which, in turn, may enhance HIV replication within macrophages or peripheral blood mononuclear cells (PBMC) (36).…”

mentioning

confidence: 99%

Mandelic Acid Condensation Polymer: Novel Candidate Microbicide for Prevention of Human Immunodeficiency Virus and Herpes Simplex Virus Entry

Herold¹,

Scordi-Bello

Cheshenko³

et al. 2002

J Virol

View full text Add to dashboard Cite

Presently marketed vaginal barrier methods are cytotoxic and damaging to the vaginal epithelium and natural vaginal flora when used frequently. Novel noncytotoxic agents are needed to protect men and women from sexually transmitted diseases. One novel candidate is a mandelic acid condensation polymer, designated SAMMA. The spectrum and mechanism of antiviral activity were explored using clinical isolates and laboratory-adapted strains of human immunodeficiency virus (HIV) and herpes simplex virus (HSV). SAMMA is highly effective against all CCR5 and CXCR4 isolates of HIV in primary human macrophages and peripheral blood mononuclear cells. SAMMA also inhibits infection of cervical epithelial cells by HSV. Moreover, it exhibits little or no cytotoxicity and has an excellent selectivity index. SAMMA, although not a sulfonated or sulfated polymer, blocks the binding of HIV and HSV to cells by targeting the envelope glycoproteins gp120 and gB-2, respectively, and also inhibits HSV entry postattachment. SAMMA is an excellent, structurally novel candidate microbicide that warrants further preclinical evaluation.

show abstract

Herpes Simplex Virus Infection Induces Replication of Human Immunodeficiency Virus Type 1

Cited by 69 publications

References 28 publications

Left out but not Forgotten: Should Closer Attention be Paid to Coinfection with Herpes Simplex Virus Type 1 and HIV?

Left out but not Forgotten: Should Closer Attention be Paid to Coinfection with Herpes Simplex Virus Type 1 and HIV?

Population Levels of Psychological Stress, Herpesvirus Reactivation and HIV

Mandelic Acid Condensation Polymer: Novel Candidate Microbicide for Prevention of Human Immunodeficiency Virus and Herpes Simplex Virus Entry

Contact Info

Product

Resources

About