Skip directly to site content Skip directly to page options Skip directly to A-Z link Skip directly to A-Z link Skip directly to A-Z link
Volume 19, Number 1—January 2013
Letter

Polyomavirus in Saliva of HIV-infected Children, Brazil

On This Page
Tables
Article Metrics
11
citations of this article
EID Journal Metrics on Scopus

Cite This Article

To the Editor: Human polyomaviruses (HPyVs) are members of the family Polyomaviridae. Nine distinct PyVs can infect humans: BKPyV, JCPyV, WUPyV, KIPyV, MCPyV, TSPyV, HPyV6, HPyV7, and HPyV9 (1). Primary infections generally occur early in life, are typically subclinical, and are followed by persistence of the virus in the person. Reactivation of infection has been associated with disease in immunocompromised persons (26). We detected the excretion of HPyV in the saliva of HIV-infected children and compared this finding with its prevalence in healthy control children to evaluate the possible association between viral infection and the stage of immunodeficiency.

Samples were collected during August 2009–June 2011 from patients attending the School of Dentistry of the Federal University of Rio de Janeiro, Brazil. Saliva samples were obtained from 60 HIV-infected children (27 (44.9%) boys, 33 (55.1%) girls), 6–13 years of age (median 9.5 years), and 60 healthy children (47.9% male, 52.1% female), 7–12 years of age (median 9.04 years). The study protocol was approved by the Ethics Committee of the Hospital Universitário Clementino Fraga Filho/University of Rio de Janeiro. The parents of all children involved in the study gave informed consent.

Virus DNA was extracted by using the Wizard Genomic DNA Purification Kit (Promega, Madison, WI, USA). Specimens were tested for HPyV by real-time PCR (7,8). For BKPyV, we used primer pair BKV-F: 5′-GGTGTAGATCAGAGGGAAAGT-3′ and BKV-R: 5′-TTGCCAGTG ATGAAGAAG C-3′. Statistical significance was assessed by p<0.05.

HPyVs were detected in 17 (28.3%) and 6 (10%) of HIV-infected and control children, respectively (Table). A higher frequency of viral infection was observed in the HIV-infected group (p = 0.01). Frequency of KIPyV infection was significantly higher among immunocompromised children (p = 0.02). No difference was observed for BKPyV, JCPyV, or WUPyV. The virus loads were similar in both groups (data not shown).

HIV-infected persons were classified into 3 immunologic categories: no evidence of immune suppression (CD4+ >500 cells/µL; n = 38), moderate suppression (CD4+ 200–499 cells/µL; n = 13), and severe suppression (CD4+ <200 cells/µL; n = 9). HPyV was more frequently detected among children with severe immunosuppression (n = 7; p<0.001). However, no significant correlation was observed between the frequency of HPyV DNA detection and the use of highly active antiretroviral therapy (HAART) (p = 0.156).

Because the immunosuppressed population is increasing around the world, the role of HPyVs as opportunistic pathogens in these persons has become a great concern (26). In this study, we found that the frequency of HPyV infections was higher among HIV-infected children than among the general pediatric population, although infection was not associated with the person’s CD4+ cell count. The viral loads were similar in both groups, suggesting that efficiency of viral replication is not related to the person’s immune status. None of the HPyV-positive children, including those with severe immunosuppression (data not shown), showed any symptoms of illness associated with these viruses, such as urinary tract, neurologic, or respiratory tract infection.

Previous studies analyzed the occurrence of HPyV infections in immunosuppressed persons with AIDS. Sharp et al. investigated the presence of WUPyV, KIPyV, and MCPyV in lymphoid tissue samples from persons with AIDS and healthy controls and found a much higher frequency of infection in the immunosuppressed group (9). Babakir-Mina et al. investigated the frequency KIPyV and WUPyV in blood of HIV-1–infected patients compared with blood donors and demonstrated that WUPyV infection was more frequent in HIV-infected patients but the frequency of infection for KIPyV was similar in both groups; they also found no association between CD4+ cells count and HPyV infection (2). Machado et al. investigated the urinary excretion of BKPyV and JCPyV among HIV-1–infected children and adolescents and healthy controls and demonstrated a significantly higher BKPyV viruria in HIV-infected patients. No difference was observed for JCPyV excretion, however, and no association was found between CD4+ values and viral shedding (3). Jeffers et al. assessed the salivary shedding of BKPyV on a cohort of healthy and HIV-immunosuppressed persons and found that BKPyV DNA levels in the saliva were significantly higher in HIV-infected patients. They also demonstrated the ability of a BKPyV to replicate in vitro in salivary gland cells and suggested that salivary glands may constitute a reservoir for BKPyV (10). Jeffers and Webster-Cyriaque, while investigating the contribution of viral infection to the pathogenesis of salivary gland diseases, detected BKPyV shedding in the saliva of HIV-positive patients with salivary gland diseases more often than in healthy controls and suggested that it played a possible role in the disease (4). In contrast, other studies did not detect BKPyV or JCPyV in saliva of either HIV-infected or healthy controls (6,7).

In this study, we detected DNA of BKPyV, JCPyV, WUPyV, and KIPyV in saliva samples of both HIV-positive and healthy control children, although the frequency of infection was significantly higher among the HIV-infected children. These findings suggest that saliva may be a route of HPyV transmission and that the oral cavity could be a site of virus replication and persistence.

Top

Acknowledgments

We thank Soluza dos Santos Gonçalves for technical assistance.

This study was supported in part by Conselho Nacional de Desenvolvimento Científico e Tecnológico, Coordenação de Aperfeiçoamento de Pessoal de Nível Superior, and, Fundação Carlos Chagas de Amparo à Pesquisa do Estado do Rio de Janeiro, Brazil. This manuscript represents a portion of a thesis submitted by T.F.R. to the Federal University of Rio de Janeiro, Brazil, as a partial fulfillment of the requirements for her doctorate.

Top

Tatiana F. Robaina1, Gabriella S. Mendes1, Fabrício J. Benati, Giselle A. Pena, Raquel C. Silva, Miguel A.R. Montes, Renata Otero, Gloria F. Castro, Fernando P. Câmara, and Norma SantosComments to Author 
Author affiliations: Author affiliation: Federal University of Rio of Janeiro, Rio de Janeiro, Brazil

Top

References

  1. Scuda  N, Hofmann  J, Calvignac-Spencer  S, Ruprecht  K, Liman  P, Kühn  J, A novel human polyomavirus closely related to the African green monkey–derived lymphotropic polyomavirus. J Virol. 2011;85:458690. DOIPubMedGoogle Scholar
  2. Babakir-Mina  M, Ciccozzi  M, Farchi  F, Bergallo  M, Cavallo  R, Adorno  G, KI and WU polyomaviruses and CD4+ cell counts in HIV-1–infected patients, Italy. Emerg Infect Dis. 2010;16:14825. DOIPubMedGoogle Scholar
  3. Machado  DM, Fink  MC, Pannuti  CS, Succi  RC, Machado  AA, do Carmo  FB, Human polyomaviruses JC and BK in the urine of Brazilian children and adolescents vertically infected by HIV. Mem Inst Oswaldo Cruz. 2011;106:9315. DOIPubMedGoogle Scholar
  4. Jeffers  L, Webster-Cyriaque  JY. Viruses and salivary gland disease (SGD): lessons from HIV SGD. Adv Dent Res. 2011;23:7983. DOIPubMedGoogle Scholar
  5. Berger  JR, Miller  CS, Mootoor  Y, Avdiushko  SA, Kryscio  RJ, Zhu  H. JC virus detection in bodily fluids: clues to transmission. Clin Infect Dis. 2006;43:e912. DOIPubMedGoogle Scholar
  6. Sundsfjord  A, Spein  AR, Lucht  E, Flaegstad  T, Seternes  OM, Traavik  T. Detection of BK virus DNA in nasopharyngeal aspirates from children with respiratory infections but not in saliva from immunodeficient and immunocompetent adult patients. J Clin Microbiol. 1994;32:13904 .PubMedGoogle Scholar
  7. Bialasiewicz  S, Whiley  DM, Lambert  SB, Nissen  MD, Sloots  TP. Detection of BK, JC, WU, or KI polyomaviruses in faecal, urine, blood, cerebrospinal fluid and respiratory samples. J Clin Virol. 2009;45:24954. DOIPubMedGoogle Scholar
  8. Agostini  HT, Ryschkewitsch  CF, Stoner  GL. Genotype profile of human polyomavirus JC excreted in urine of immunocompetent individuals. J Clin Microbiol. 1996;34:15964 .PubMedGoogle Scholar
  9. Sharp  CP, Norja  P, Anthony  I, Bell  JE, Simmonds  P. Reactivation and mutation of newly discovered WU, KI, and Merkel cell carcinoma polyomaviruses in immunosuppressed individuals. J Infect Dis. 2009;199:398404. DOIPubMedGoogle Scholar
  10. Jeffers  LK, Madden  V, Webster-Cyriaque  J. BK virus has tropism for human salivary gland cells in vitro: implications for transmission. Virology. 2009;394:18393. DOIPubMedGoogle Scholar

Top

Table

Top

Cite This Article

DOI: 10.3201/eid1901.120563

1These authors contributed equally to this article.

Related Links

Top

Table of Contents – Volume 19, Number 1—January 2013

EID Search Options
presentation_01 Advanced Article Search – Search articles by author and/or keyword.
presentation_01 Articles by Country Search – Search articles by the topic country.
presentation_01 Article Type Search – Search articles by article type and issue.

Top

Comments

Please use the form below to submit correspondence to the authors or contact them at the following address:

Norma Santos, Departamento de Virologia, Instituto de Microbiologia, Universidade Federal do Rio de Janeiro, Cidade Universitária, CCS–Bl. I, Ilha do Fundão Rio de Janeiro–RJ, 21.941-972, Brazil

Send To

10000 character(s) remaining.

Top

Page created: December 20, 2012
Page updated: December 20, 2012
Page reviewed: December 20, 2012
The conclusions, findings, and opinions expressed by authors contributing to this journal do not necessarily reflect the official position of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. Use of trade names is for identification only and does not imply endorsement by any of the groups named above.
file_external