Prospective study of human herpesvirus 8 oral shedding, viremia, and serological status among human immunodeficiency virus seropositive and seronegative individuals in Sao Paulo, Brazil

Carregando...
Imagem de Miniatura
Citações na Scopus
7
Tipo de produção
article
Data de publicação
2017
Título da Revista
ISSN da Revista
Título do Volume
Editora
TAYLOR & FRANCIS LTD
Citação
JOURNAL OF ORAL MICROBIOLOGY, v.9, article ID 1384287, 6p, 2017
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Human herpesvirus 8 (HHV-8) is a gamma-herpesvirus and etiological agent of all forms of Kaposi sarcoma (KS). Saliva may play an important role in HHV-8 transmission in specific populations. Little is known about HHV-8 oral shedding pattern and the possible correlation with the HHV-8 serological profile and viremia. A prospective study was conducted of HHV-8 salivary excretion among human immunodeficiency virus HIV-seronegative (n = 47) and -seropositive (n = 44) homosexual men and HIV-seropositive women (n = 32) over a 6-month period with monthly HHV-8 serologies (immunofluorescence assays to identify antibodies to latent and lytic HHV-8 viral proteins, and a whole-virus HHV-8 enzyme-linked immunosorbent assay [ELISA]), monthly HHV-8 DNA serum/plasma detection, and daily self-collected oral rinses for HHV-8-DNA detection using real-time polymerase chain reaction. HHV-8 seropositivity was 51.1%, 63.6%, and 37.5%, in the three studied groups. There was no case of HHV-8 DNA detection in serum/plasma. Intermittent detection of oral HHV-8 DNA was observed during 5.1% (110/2,160) of visits among 28% (18/64) of HHV-8-seropositive individuals, all of whom were males and HHV-8 ELISA seropositive. In immunologically controlled populations of Brazil, HHV-8 oral shedding was limited to HHV-8-seropositive men, occurred infrequently and intermittently, and was not linked to HHV-8 viremia, suggesting a limited potential for oral or blood transmission.
Palavras-chave
HHV-8, oral shedding, Kaposi sarcoma, HIV
Referências
  1. Casper C, 2004, JAIDS-J ACQ IMM DEF, V35, P233, DOI 10.1097/00126334-200403010-00003
  2. Casper C, 2007, J INFECT DIS, V195, P30, DOI 10.1086/509621
  3. de Souza VAUF, 2007, J INFECT DIS, V196, P844, DOI 10.1086/520549
  4. Del Mistro A, 2012, SEX TRANSM DIS, V39, P894, DOI 10.1097/OLQ.0b013e31826ef2da
  5. Ignacio RAB, 2016, INFECT AGENTS CANCER, V11, DOI 10.1186/s13027-016-0052-2
  6. Johnston C, 2009, PLOS ONE, V4, DOI 10.1371/journal.pone.0004222
  7. Levi JE, 2011, PLOS ONE, V6, DOI 10.1371/journal.pone.0023546
  8. Nascimento MC, 2007, J CLIN MICROBIOL, V45, P715, DOI 10.1128/JCM.01264-06
  9. Pauk J, 2000, NEW ENGL J MED, V343, P1369, DOI 10.1056/NEJM200011093431904
  10. Phipps W, 2014, J MED VIROL, V86, P1759, DOI 10.1002/jmv.23941
  11. Pierrotti LC, 2005, SEX TRANSM DIS, V32, P57, DOI 10.1097/01.olq.0000148300.33428.6e
  12. Qu LR, 2010, TRANSFUSION, V50, P1050, DOI 10.1111/j.1537-2995.2009.02559.x
  13. Souza VAUF, 2004, BRAZ J MED BIOL RES, V37, P123, DOI 10.1590/S0100-879X2004000100017
  14. Taylor MM, 2004, J INFECT DIS, V190, P484, DOI 10.1086/421466
  15. Tozetto-Mendoza TR, 2018, J INVESTIG CLIN DENT, V9, DOI 10.1111/jicd.12278
  16. Vamvakas EC, 2011, TRANSFUS MED REV, V25, P47, DOI 10.1016/j.tmrv.2010.08.006
  17. Vitale F, 2000, EPIDEMIOL INFECT, V125, P671, DOI 10.1017/S0950268800004726
  18. Widmer IC, 2006, JAIDS-J ACQ IMM DEF, V42, P420, DOI 10.1097/01.qai.0000226790.31463.e6