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Occult Hepatitis B Virus Infections (Often with Human Herpesvirus 7 Co-Infection) Detected in Pityriasis rosea Patients: A Pilot Study

BACKGROUND: The etiopathogenesis of Pityriasis rosea (PR), a papulo-squamous skin disease, remains elusive and hypothesized to be caused primarily by human herpesvirus (HHV) 6 or 7 or immune dysfunction. AIMS: The recent increasing incidences of hepatitis B virus (HBV) infections, including asymptom...

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Detalles Bibliográficos
Autores principales: De, Abhishek, Roy, Subrata, Sukla, Soumi, Ansari, Asad, Biswas, Subhajit
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5724307/
https://www.ncbi.nlm.nih.gov/pubmed/29263533
http://dx.doi.org/10.4103/ijd.IJD_235_17
Descripción
Sumario:BACKGROUND: The etiopathogenesis of Pityriasis rosea (PR), a papulo-squamous skin disease, remains elusive and hypothesized to be caused primarily by human herpesvirus (HHV) 6 or 7 or immune dysfunction. AIMS: The recent increasing incidences of hepatitis B virus (HBV) infections, including asymptomatic occult HBV infections (OBIs), in a densely populated city in India, prompted us to investigate whether PR patients (from varied socioeconomic and immune status) harbor the underlying HBV infections. These cases were also investigated for HHV 6 and 7 infections. MATERIALS AND METHODS: DNA from ethylenediaminetetraacetic acid blood samples from PR-diagnosed individuals (n = 13; mostly young adults) and healthy controls (n = 11) were subjected to virus gene-specific polymerase chain reactions (PCRs) for HBV and HHV 6 and 7. PCR products of expected length, when observed, were sequenced (bidirectional) using overlapping primers. Sequences were identified by NCBI BLAST and analyzed by multiple sequence alignment and phylogenetic studies. The blood samples were tested for HBsAg by EIA. RESULTS: In 5/13 PR samples, only HBV DNA (4/5 being HBsAg negative) was detected, providing first-time evidence that PR may be manifested in asymptomatic HBV carriers. 6/13 cases were HHV 7 (not HHV 6) DNA positive, providing confirmatory molecular genetic evidence for the first time of PR association with HHV 7 from India. Surprisingly, 5/6 HHV 7-positive PR cases were also HBV positive. Overall, 10/13 PR samples showed evidence of HBV infection. 8/13 were OBI, harboring at least one OBI-signature S protein mutation. All healthy controls were HBsAg EIA and PCR negative. CONCLUSIONS: 77% of PR patients presented the evidence of underlying HBV infection (genotype D2), suggestive of horizontal HBV transmission. This warrants for mass HBV vaccination. PR patients should be tested for underlying virus infections for appropriate therapy and management.