Vol 61, No 6 (2016)

Twenty years ago in the South Chinese province of Guangdong the epizooty of highly pathogenic avian influenza (HPAI) H5N1 virus, which has laid the foundation of the largest epizooty in the contemporary history, has flashed. Hemagglutinin of prototype A/goose/Guangdong/1/1996 (H5N1) changing many times and generating new genetic subgroups participated in various reassortations; it still exists today. The present review is devoted to the retrospective analysis of HPAI/H5N1evolution for the last twenty years in the territory of Eurasia, Africa and America. The basis for the discussion is ecological model according to which new genetic variants are formed in the migration pathways with close contacts between different bird populations and in the overwintering areas where the maximum values of the immune layer occur; amplification of virus variants occurs in nesting areas among juvenile populations. The updated system of designations of genetic groups introduced by WHO/OIE/FAO H5 Evolution Working Group in 2015 is used.

Reassortants with surface antigens from potentially pandemic A/H2N2 and A/H7N9 influenza viruses were created on the basis of attenuated and highly reproductive A/Hong Kong/1/68/162/35(H3N2) donor virus obtained in the Research institute of influenza. High reproductive activity of reassortant viruses and immunogenicity of live and inactivated influenza vaccines based on these viruses indicate the possibility to use obtained reassortants for production of live and inactivated vaccines against potentially pandemic influenza A viruses.

The study involved 500 patients with LSIL (low grade squamous intraepithelial lesion), HSIL (high grade squamous intraepithelial lesion), stage I-IV cervical cancer, infected with human papillomavirus (HPV), as well as 235 women without pathological changes in cervical mucosa. The comprehensive survey included colposcopy, cytological and histological analysis, detection and genotyping of high-risk human papillomavirus. Viral load and physical status of HPV16 DNA was evaluated in cases of mono-infection (n = 148). The prevalence of virus-positive cases among the patients with LSIL/NSIL, cervical cancer patients and healthy women was 69.2%, 76.7% and 51.9%, respectively. An association between the severity of disease and high viral load was revealed. The frequency of integrated DNA was strongly increased in patients with a high viral load. The frequency of episomal forms was either reduced or not detecteable in patients with high viral load as compared to patients with low viral load. It is reasonable to suggest that a high HPV16 viral load may cause an increase in the frequency of integration of virus DNA into the cellular/host genome. This suggests that a high HPV16 viral load may be considered as a risk factor for prognosis of cervical intraepithelial neoplasia and cervical cancer.

Data on hepatitis B (HBV) and c (HCV) viruses interference in hematological patients are described. Patients with a hematological malignancy are at high risk of HBV and HCV infection as recipients of multiple transfusions. Results of the laboratory testing of 339 blood samples of patients treated at the National Research center for Hematology, Russian Federation, were studied. Among these patients, HBV/HCV coinfection markers were observed in 153 patients; HBV markers only, in 76 patients; HCV markers only, in 110 patients. The vast majority of coinfected patients had HBV DNA in blood (significantly more in HBsAg-negative patients: 100% vs. 82.8%, p = 0. 0005). HBsAg-negative coinfected patients had low HBV DNA levels (102-103ME/ml) and reduced (or completely absent) HCV RNA levels. The virus interference leads to a decrease in the viral nucleic acid concentrations. Thus, virus detection should include implementation of high sensitive molecular techniques (such as real-time PCR), and an enhanced set of serological HBV markers along with routine screening methods (HBsAg, anti-HCV).

Results of comprehensive ELISA tests of blood serum for the presence of IgM-, IgA-, and IgG-antibodies to herpes simplex virus types 1 and 2, cytomegalovirus, Epstein-Barr virus, human herpesvirus 6, human herpes virus 8 type, Chlamydia trachomatis in 38 patients with uveal melanoma are presented. The polymerase chain reaction was used to detect DNA of these pathogens in tumor biopsies, vitreous body of 10 enucleated eyes, as well as in plasma IgG-antibodies to HHV 6 were revealed in 50% of patients; IgG-antibodies to HHV 8, in 5.3% of patients. Among the 16 patients with uveal melanoma at advanced stages, 6 patients had antibodies indicative of EBV reactivation (1.2-3.3). Chlamydia trachomatis genome was detected in both biopsies; in one of them, in conjunction with EBV and CMV DNA . Tissue samples from the identified infectious agents were related only to the spindle-cell histologic type AB of uveal melanoma. In plasma, genomes of pathogens were not determined. The results indicate the presence of infectious agents in patients with uveal melanoma and require further study of the pathogenetic role of infections in the pathogenesis of uveal melanoma.