Antibody to Herpes Simplex Virus Type 2 as a Marker of Sexual Risk Behavior in Rural Tanzania

Obasi, Angela; Mosha, Frank; Quigley, Maria A.; Sekirassa, Zebedayo; Gibbs, T; Munguti, Katua; Todd, Jim; Grosskurth, Heiner; Mayaud, Philippe; Changalucha, John; Brown, David; Mabey, David; Hayes, Richard

doi:10.1086/314555

Cited by 156 publications

(104 citation statements)

References 29 publications

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“…The prevalence at older ages was low (below 10%). These observations are consistent with the natural history of HSV-1 and HSV-2 infections as reported in sub-Saharan Africa or elsewhere, with near universal infection by HSV-1 in early childhood and rapid rise of HSV-2 infection around the time of puberty and beginning of sexual activity (5,16,18).…”

supporting

confidence: 90%

Performance of the BioPlex 2200 Multiplexing Immunoassay Platform for the Detection of Herpes Simplex Virus Type 2 Specific Antibodies in African Settings

Goff

Grésenguet

Gody

et al. 2011

Clin. Vaccine Immunol.

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supporting

confidence: 90%

Performance of the BioPlex 2200 Multiplexing Immunoassay Platform for the Detection of Herpes Simplex Virus Type 2 Specific Antibodies in African Settings

Goff

Grésenguet

Gody

et al. 2011

Clin. Vaccine Immunol.

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“…In rural populations in Africa sampled randomly, the prevalence of HSV-2 antibodies was 75% in women >25 years and 60% in men >30 years in Mwanza, Tanzania 40 and 68% overall in Masaka, Uganda. 41 High rates (59%) are also reported in commercial sex workers in Nigeria.…”

Section: Hsv In Developing Countries: the Presentmentioning

confidence: 98%

Increasing prevalence of genital herpes in developing countries: implications for heterosexual HIV transmission and STI control programmes

O’Farrell

1999

Sexually Transmitted Infections

100

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Background:The recognition that sexually transmitted infections (STI) facilitate HIV transmission among heterosexuals has led to a rejuvenated focus on improving STI control as a component of HIV prevention programmes in developing countries. While eVorts so far have focused mainly on all STI, there is increasing evidence that genital ulcers facilitate a considerable proportion of HIV transmission among heterosexuals and that this eVect has been underestimated. This paper focuses on the epidemiology of genital herpes in developing countries past and present. Objectives: To review the scientific literature about the epidemiology of genital herpes in developing countries and discuss the implications of the findings for STI control and HIV prevention programmes. Search methodology: A Medline search for June 1966 to August 1999 using the keywords, genital herpes, STD and developing countries, and genital ulcers in MeSH and free text. Abstract books from recent international AIDS conferences and other international STD conferences were reviewed. The annual reports of the medical oYcers of heath for Harare 1982 and Durban 1989 were reviewed to detect trends in genital herpes diagnoses. Findings: Genital herpes, formerly regarded as a minor STI in most developing countries, has now emerged as a leading cause of genital ulceration in many countries where syphilis and chancroid were more prevalent previously. This increased recognition of genital herpes reflects both a change in the pattern of STI epidemiology through a decline in syphilis and chancroid as a response to HIV control programmes and improved techniques for diagnosing herpetic infection. Countries with significant heterosexual HIV epidemics also appear to have rapidly increasing numbers of genital herpes cases. Conclusions:The emergence of this herpes epidemic must be addressed through innovative strategies that will be viable, sustainable, acceptable, and eVective in developing countries. In countries where genital herpes is a significant problem, local adaptation of WHO treatment algorithms should be made. STI service providers should be trained about issues around the transmission of herpes and how best to advise clients about dealing with, and recognising, recurrences. The eVectiveness of antiviral treatment for genital herpes should be investigated in core groups at high risk of HIV. (Sex Transm Inf 1999;75:377-384)

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“…From their site of latency in the ganglia, HSV-1 and HSV-2 periodically reactivate to cause recurrent shedding and mucosal disease (1). HSV-2 infects primarily the anogenital epithelium of nearly one in five adults in the United States (2) and up to 75% of adults worldwide (3,4). HSV-2 also causes serious and sometimes fatal neurologic disease in babies born to women experiencing peripartum primary or recurrent infection (5).…”

mentioning

confidence: 99%

Up to Four Distinct Polypeptides Are Produced from the γ34.5 Open Reading Frame of Herpes Simplex Virus 2

Korom

Davis

Morrison

2014

J Virol

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The herpes simplex virus 1 (HSV-1) ICP34.5 protein strongly influences neurovirulence and regulates several cellular antiviral responses. Despite the clinical importance of HSV-2, relatively little is known about its ICP34.5 ortholog. We found that HSV-2 produces up to four distinct forms of ICP34.5 in infected cells: a full-length protein, one shorter form sharing the N terminus, and two shorter forms sharing the C terminus. These forms appeared with similar kinetics and accumulated in cells over much of the replication cycle. We confirmed that the N-terminal form is translated from the primary unspliced transcript to a stop codon within the intron unique to HSV-2 ␥34.5. We found that the N-terminal form was produced in a variety of cell types and by 9 of 10 clinical isolates. ICP27 influenced but was not required for expression of the N-terminal form. Western blotting and reverse transcription-PCR indicated the C-terminal forms did not contain the N terminus and were not products of alternative splicing or internal transcript initiation. Expression plasmids encoding methionine at amino acids 56 and 70 generated products that comigrated in SDS-PAGE with the C1 and C2 forms, respectively, and mutation of these sites abolished C1 and C2. Using a recombinant HSV-2 encoding hemagglutinin (HA)-tagged ICP34.5, we demonstrated that the C-terminal forms were also produced during infection of many human and mouse cell types but were not detectable in mouse primary neurons. The protein diversity generated from the HSV-2 ␥34.5 open reading frame implies additional layers of cellular regulation through potential independent activities associated with the various forms of ICP34.5. IMPORTANCEThe herpes simplex virus 1 (HSV-1) protein ICP34.5, encoded by the ␥34.5 gene, interferes with several host defense mechanisms by binding cellular proteins that would otherwise stimulate the cell's autophagic, translational-arrest, and type I interferon responses to virus infection. ICP34.5 also plays a crucial role in determining the severity of nervous system infections with HSV-1 and HSV-2. The HSV-2 ␥34.5 gene contains an intron not present in HSV-1 ␥34.5. A shorter N-terminal form of HSV-2 ICP34.5 can be translated from the unspliced ␥34.5 mRNA. Here, we show that two additional forms consisting of the C-terminal portion of ICP34.5 are generated in infected cells. Production of these N-and C-terminal forms is highly conserved among HSV-2 strains, including many clinical isolates, and they are broadly expressed in several cell types, but not mouse primary neurons. Multiple ICP34.5 polypeptides add additional complexity to potential functional interactions influencing HSV-2 neurovirulence.

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Antibody to Herpes Simplex Virus Type 2 as a Marker of Sexual Risk Behavior in Rural Tanzania

Cited by 156 publications

References 29 publications

Performance of the BioPlex 2200 Multiplexing Immunoassay Platform for the Detection of Herpes Simplex Virus Type 2 Specific Antibodies in African Settings

Performance of the BioPlex 2200 Multiplexing Immunoassay Platform for the Detection of Herpes Simplex Virus Type 2 Specific Antibodies in African Settings

Increasing prevalence of genital herpes in developing countries: implications for heterosexual HIV transmission and STI control programmes

Up to Four Distinct Polypeptides Are Produced from the γ34.5 Open Reading Frame of Herpes Simplex Virus 2

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