Herpes Simplex Virus Type 2 Acquisition During Recent HIV Infection Does Not Influence Plasma HIV Levels

Frost, Simon D. W.; Poon, Art F. Y.; Looney, David J.; Rostami, Sherry M; Pacold, Mary E.; Richman, Douglas D.; Smith, Davey M.

doi:10.1097/qai.0b013e318163bd87

Cited by 10 publications

(13 citation statements)

References 13 publications

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“…Of these, eight assessed the association between HSV-2 infection and PVL (Table 2a); three were cohort studies [21,39,40], four were cross-sectional [41–44] and one was a nested case-control study [45]. Cross-sectional and case-control studies compared PVL among participants with or without HSV-2, and cohort studies measured PVL through the course of a HSV-2 clinical episode.…”

Section: Resultsmentioning

confidence: 99%

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The role of coinfections in HIV epidemic trajectory and positive prevention

Barnabas

Webb

Weiss

et al. 2011

Aids

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Objectives Recurrent or persistent co-infections may increase HIV viral load (VL) and, consequently, risk of HIV transmission, thus increasing HIV incidence. We evaluated the association between malaria, HSV-2 and TB co-infections and their treatment on HIV VL. Design Systematic review and meta-analysis of the association of malaria, HSV-2 and tuberculosis co-infections and their treatment on HIV VL. Methods PunMed and Embase databases were searched to February 10th 2010 for studies in adults that reported HIV plasma and/or genital VL by co-infection status or treatment. Meta-analyses were conducted using random-effects models. Results Forty-five eligible articles were identified (6 malaria, 20 HSV-2 and 19 tuberculosis). There was strong evidence of increased HIV VL with acute malaria (0.67 log10 copies/mL, 95% CI: 0.15, 1.19) and decreased VL following treatment (−0.37 log10 copies/mL, 95% CI: −0.70, −0.04). Similarly, HSV-2 infection was associated with increased HIV VL (0.18 log10 copies/mL, 95% CI: 0.01, 0.34), which decreased with HSV suppressive therapy (−0.28 log10 copies/mL, 95% CI: −0.36, − 0.19). Active tuberculosis was associated with increased HIV VL (log10 copies/mL 0.40, 95% CI: 0.13–0.67), but there was no association between tuberculosis treatment and VL reduction (log10 copies/mL −0.02, 95% CI −0.19, 0.15). Conclusions Co-infections may increase HIV VL in populations where they are prevalent, thereby facilitating HIV transmission. These effects may be reversed with treatment. However, to limit HIV trajectory and optimize positive prevention for HIV-infected individuals pre-ART, we must better understand the mechanisms responsible for augmented VL and the magnitude of VL reduction required, and retune treatment regimens accordingly

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Section: Resultsmentioning

confidence: 99%

“…The effect of incident HSV-2 infection (i.e. recent seroconversion) on PVL was reported in two articles, neither of which found any association [21,39]. Eight studies examined the association between prevalent HSV-2 infection and HIV PVL.…”

Section: Resultsmentioning

confidence: 99%

The role of coinfections in HIV epidemic trajectory and positive prevention

Barnabas

Webb

Weiss

et al. 2011

Aids

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“…20 Likewise, studies among women attending STD clinics in the U.S. have reported incidence ranging from 5.7–20.5 per 100 woman years 21, 22 and similarly 4.9–14.2 per 100 person years in other populations. 6, 23, 24 …”

Section: Discussionmentioning

confidence: 99%

Incidence, Prevalence, and Epidemiology of Herpes Simplex Virus-2 in HIV-1-Positive and HIV-1-Negative Adolescents

Sudenga

Kempf²,

McGwin

et al. 2012

Sexually Transmitted Diseases

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Background Several studies have assessed risk factors associated with herpes simplex virus-2 (HSV-2) prevalence in adults; however, few have focused on HSV-2 incidence, particularly in adolescents. The objective of this study was to determine HSV-2 prevalence and incidence and associated risk factors in a HIV-1-positive and at risk HIV-1-negative adolescent population. Methods Sera were tested for HSV-2 antibodies in 518 adolescents in the Reaching for Excellence in Adolescent Care and Health (REACH) cohort at baseline and again at the final follow-up visit. Prevalence at baseline and incidence (per person years) of HSV-2 infection were calculated. Furthermore, among HIV-1-positive individuals, a subgroup analysis was performed to assess risk factors for HSV-2 infection. Conditional logistic regression was used to estimate odds ratios (OR) and p-values (p) for associations between CD4+ T-cell (CD4+) count, HIV-1 viral load (VL), and HSV-2 acquisition, adjusting for antiretroviral therapy use, other sexually transmitted infections, gender, race, and number of sexual partners. Results At baseline, 179 (35%) subjects were HSV-2 positive, with an additional 47 (16%) new cases being identified during a median follow-up time of 1.95 years and an incidence rate of 7.35 cases per 100 person years (py). Several risk factors were associated with HSV-2 prevalence (being female, non-Hispanic, uncertainty of sexual preference, and HIV-1 positive) and incidence (using drugs, alcohol, and number of new sexual partners). Among HIV-1 positives, an increase in CD4+ count by 50 cell/mm3 (OR, 1.17; 95% CI 1.04–1.31, p=0.008) was associated with HSV-2 acquisition. Conclusions The high prevalence and incidence of HSV-2 infection among adolescents, compared to the general population at this age group suggests a critical need for screening and preventive programs among this targeted group.

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“…Such modulations of HSV-2 severity in those with preexisting HSV-1 antibodies may be particularly important given the above-mentioned later age of HSV-1 seroincidence in some settings (56), because an increasing proportion of individuals may be expected to acquire primary HSV-2 infection (ie, incident HSV-2 in the absence of prior HSV-1 antibodies). One study (10) reported that incident HSV-2 infection in recently HIV-infected individuals was not associated with significant changes in HIV viral load or CD4 cell count levels, but pre-existing HSV-1 serology was not documented. Most incident cases of HSV-2 infection in that study likely had preexisting HSV-1 antibodies, because nine of 10 cases were asymptomatic.…”

Section: Hsv-1 May Modulate the Course Of Incident Hsv-2 Infectionmentioning

confidence: 99%

“…In comparison, the prevalence of HSV-1 and HSV-2 in the general population is considerably lower, at roughly 70% to 100% and 6% to 50%, respectively (8,9). The incidence of HSV-2 is also higher in HIV-infected populations, estimated at 18 to 74 per 1000 person-years versus 8.4 per 1000 person-years (7,10,11). Both HSV-2 and HSV-1 are enveloped DNA viruses that cause lifelong incurable infections.…”

mentioning

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

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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.

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Herpes Simplex Virus Type 2 Acquisition During Recent HIV Infection Does Not Influence Plasma HIV Levels

Cited by 10 publications

References 13 publications

The role of coinfections in HIV epidemic trajectory and positive prevention

The role of coinfections in HIV epidemic trajectory and positive prevention

Incidence, Prevalence, and Epidemiology of Herpes Simplex Virus-2 in HIV-1-Positive and HIV-1-Negative Adolescents

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

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