1. [The role of herpesviruses in development of diseases of the urogenital tract and infertility in women].
- Author
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Kushch AA, Kisteneva LB, Klimova RR, and Cheshik SG
- Subjects
- Female, Herpes Genitalis epidemiology, Herpesviridae classification, Herpesviridae genetics, Herpesvirus 1, Human pathogenicity, Herpesvirus 2, Human pathogenicity, Herpesvirus 6, Human pathogenicity, Humans, Infertility, Female epidemiology, Pregnancy, Premature Birth epidemiology, Premature Birth virology, Reproductive Tract Infections epidemiology, Herpes Genitalis virology, Herpesviridae pathogenicity, Infertility, Female virology, Reproductive Tract Infections virology
- Abstract
This review presents the data on the spreading of all known human herpesviruses (НHVs) in female urogenital tract. According to the WHO almost 500 million people worldwide suffer from genital infection caused by НHVs. НHVs were detected in various inflammatory diseases of female upper and lower genital tract (vaginitis and cervicitis), in extrauterine pregnancy (in fallopian tubes), in infertility (cervical channel, endometrium and ovaries). Herpes simplex virus 1 (HSV‑1) was identified for the first time in oocytes after failed in vitro fertilization (IVF). НHVs produce negative effect on the entire reproductive process from conception to childbirth. It was established that HSV, cytomegalovirus (CMV) and human herpesvirus 6 (HHV-6) markedly increase the risk of spontaneous abortion, preterm birth and stillbirth. Intrauterine НHV infection is a major cause of congenital malformations. Data on humoral and cell immunity in genital herpesvirus infections (НHVI) are also reviewed. Intravaginal HSV‑2 infection changes cell composition of vaginal mucosa, i.e., together with cells mobilized from the blood, protective role is performed by resident memory T‑cells (TRM), natural killer cells (NK‑cells) and regulatory T‑cells (Treg) whose function consists in maintaining the balance of the activities of lymphocytes. Constant НHVI spreading is largely explained by transition of primary infection to potentially reactivating latent form, since latent virus is unavailable to immune recognition and medicines. The genome editing system CRISPR/Cas9 can recognize and modify not only active but also latent viruses. The promising pilot results with the use of this system offer the possibility of developing innovative technologies for НHV elimination and НHVI eradication.
- Published
- 2021
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