Objective. To evaluate the prevalence of HSV-1 and HSV-2 in pregnant and nonpregnant women, testing the correlation between DNA of the viruses with colposcopic and/or cytological changes, and evaluate association with sociodemographic characteristics and sexual activity. Methods. Included in this study were 106 pregnant and 130 nonpregnant women treated at primary health care units of Natal, Brazil, in the period 2010-2011. The patients were examined by colposcopy, and two cervical specimens were collected: one for cytology examination and another for analysis by PCR for detection of HSV-1 and HSV-2. Results. HSV-1 alone was detected in 16.0% of pregnant and 30.0% of nonpregnant women. For HSV-2, these rates were 12.3% and 15.5%, respectively. HSV-2 had a higher correlation with cytology and/or colposcopy changes than HSV-1 did. Genital HSV-1 infection was not associated with any of the variables tested, whereas HSV-2 infection was associated with ethnicity, marital status, and number of sexual partners. Conclusions. The prevalence of HSV-1 was higher than that observed for HSV-2 in both pregnant and nonpregnant women. The genital infection by HSV-2 was higher in women with changed colposcopy and/or cytology, and it was associated with ethnicity, marital status, and number of sexual partners. 1. Introduction Herpes simplex virus (HSV) is a neurotropic virus that has a large linear, double-stranded DNA genome protected by a capsid with icosahedral symmetry surrounded by an envelope consisting of a lipid bilayer with embedded glycoproteins, having yet a proteinaceous region between the capsid and envelope called tegument [1]. The HSV belongs to the family of Herpesviridae, subfamily Alphaherpesvirinae, and genus Simplex virus [2, 3]. It is a virus that has a very complex life cycle and stands out as one of the most common pathogens in the etiology of sexually transmitted diseases worldwide [4]. HSV infects the mucosa of the mouth, eyes, and the human anogenital tract. After primary infection, the virus replicates productively within mucosal epithelial cells and enters sensory neurons via nerve termini. The virus is then transported to neuronal cell bodies where latency is established. The virus can remain in this latent state indefinitely but can be reactivated at any time during the lifetime of the host [4, 5]. During latent infection, no infectious virus is produced from infected cells, symptoms are absent in the host, and the transmission does not occur. However, reactivation can occur only in some cells, in the absence of symptoms, enabling the
References
[1]
K. Grünewald, P. Desai, D. C. Winkler et al., “Three-dimensional structure of herpes simplex virus from cryo-electron tomography,” Science, vol. 302, no. 5649, pp. 1396–1398, 2003.
[2]
E. Anzivino, D. Fioriti, M. Mischitelli et al., “Herpes simplex virus infection in pregnancy and in neonate: status of art of epidemiology, diagnosis, therapy and prevention,” Virology Journal, vol. 6, article 40, 2009.
[3]
G. Straface, A. Selmin, V. Zanardo, M. de Santis, A. Ercoli, and G. Scambia, “Herpes simplex virus infection in pregnancy,” Infectious Disease in Obstetrics and Gynecology, vol. 2012, Article ID 385697, 6 pages, 2012.
[4]
K. C. Pe？a, M. E. Adelson, E. Mordechai, and J. A. Blaho, “Genital herpes simplex virus type 1 in women: detection in cervicovaginal specimens from gynecological practices in the United States,” Journal of Clinical Microbiology, vol. 48, no. 1, pp. 150–153, 2010.
[5]
M. P. Nicoll, J. T. Proen？a, and S. Efstathiou, “The molecular basis of herpes simplex virus latency,” FEMS Microbiology Reviews, vol. 36, no. 3, pp. 684–705, 2012.
[6]
G. Paz-Bailey, M. Ramaswamy, S. J. Hawkes, and A. M. Geretti, “Herpes simplex virus type 2: epidemiology and management options in developing countries,” Sexually Transmitted Infections, vol. 83, no. 1, pp. 16–22, 2007.
[7]
J. S. Smith and N. J. Robinson, “Age-specific prevalence of infection with herpes simplex virus types 2 and 1: a global review,” Journal of Infectious Diseases, vol. 186, supplement 1, pp. S3–S28, 2002.
[8]
V. S. S. Pereira, R. N. C. Moizeis, T. A. A. M. Fernandes, J. M. G. Araújo, R. V. Meissner, and J. V. Fernandes, “Herpes simplex virus type 1 is the main cause of genital herpes in women of Natal, Brazil,” European Journal of Obstetrics Gynecology and Reproductive Biology, vol. 161, no. 2, pp. 190–193, 2012.
[9]
S. Drake, S. Taylor, D. Brown, and D. Pillay, “Regular rerview: improving the care of patients with genital herpes,” The British Medical Journal, vol. 321, no. 7261, pp. 619–623, 2000.
[10]
D. W. Kimberlin and D. J. Rouse, “Clinical practice. Genital herpes,” The New England Journal of Medicine, vol. 350, no. 19, pp. 1970–1977, 2004.
[11]
L. Corey and A. Wald, “Maternal and neonatal herpes simplex virus infections,” The New England Journal of Medicine, vol. 361, no. 14, pp. 1328–1385, 2009.
[12]
H. H. Handsfield, A. B. Waldo, Z. A. Brown et al., “Neonatal herpes should be a reportable disease,” Sexually Transmitted Diseases, vol. 32, no. 9, pp. 521–525, 2005.
[13]
D. Solomon, D. Davey, R. Kurman et al., “The 2001 Bethesda system: terminology for reporting results of cervical cytology,” The Journal of the American Medical Association, vol. 287, no. 16, pp. 2114–2119, 2002.
[14]
R. K. Saiki, S. Scharf, F. Faloona et al., “Enzymatic amplification of β-globin genomic sequences and restriction site analysis for diagnosis of sickle cell anemia,” Science, vol. 230, no. 4732, pp. 1350–1354, 1985.
[15]
C. J. Sanguinetti, E. D. Neto, and A. J. G. Simpson, “Rapid silver staining and recovery of PCR products separated on polyacrylamide gels,” BioTechniques, vol. 17, no. 5, pp. 914–921, 1994.
[16]
G. Lucotte, C. Bathelier, V. Lespiaux, C. Bali, and T. Champenois, “Detection and genotyping of herpes simplex virus types 1 and 2 by polymerase chain reaction,” Molecular and Cellular Probes, vol. 9, no. 5, pp. 287–290, 1995.
[17]
L. I. González-Villase？or, “A duplex PCR assay for detection and genotyping of Herpes simplex virus in cerebrospinal fluid,” Molecular and Cellular Probes, vol. 13, no. 4, pp. 309–314, 1999.
[18]
G. L. Westhoff, S. E. Little, and A. B. Caughey, “Herpes simplex virus and pregnancy: a review of the management of antenatal and peripartum herpes infections,” Obstetrical and Gynecological Survey, vol. 66, no. 10, pp. 629–638, 2011.
[19]
Z. Samra, E. Scherf, and M. Dan, “Herpes simplex virus type 1 is the prevailing cause of genital herpes in the Tel Aviv area, Israel,” Sexually Transmitted Diseases, vol. 30, no. 10, pp. 794–796, 2003.
[20]
B. L. Halpern-Felsher, J. L. Cornell, R. Y. Kropp, and J. M. Tschann, “Oral versus vaginal sex among adolescents: perceptions, attitudes, and behavior,” Pediatrics, vol. 115, no. 4, pp. 845–851, 2005.
[21]
M. Dan, O. Sadan, M. Glezerman, D. Raveh, and Z. Samra, “Prevalence and risk factors for herpes simplex virus type 2 infection among pregnant women in Israel,” Sexually Transmitted Diseases, vol. 30, no. 11, pp. 835–838, 2003.
[22]
H. Weiss, “Epidemiology of herpes simplex virus type 2 infection in the developing world,” Herpes, vol. 11, supplement 1, pp. 24A–35A, 2004.
[23]
I. D. Kim, H. S. Chang, and K. J. Hwang, “Herpes simplex virus 2 infection rate and necessity of screening during pregnancy: a clinical and seroepidemiologic study,” Yonsei Medical Journal, vol. 53, no. 2, pp. 401–407, 2012.
[24]
ACOG Committee on Practice Bulletins-Gynecology, “ACOG practice bulletin: clinical management guidelines for obstetrician-gynecologists, number 57, November 2004. Gynecologic herpes simplex virus infections,” Obstetrics and Gynecology, vol. 104, no. 5, pp. 1111–1118, 2004.
[25]
R. Engelberg, D. Carrell, E. Krantz, L. Corey, and A. Wald, “Natural history of genital herpes simplex virus type 1 infection,” Sexually Transmitted Diseases, vol. 30, no. 2, pp. 174–177, 2003.
[26]
E. Tronstein, C. Johnston, M. L. Huang et al., “Genital shedding of herpes simplex virus among symptomatic and asymptomatic persons with HSV-2 infection,” The Journal of the American Medical Association, vol. 305, no. 14, pp. 1441–1449, 2011.
