Forough Tavakoli; Afagh Moattari; Mahmoud Shamsi Shahr Abadi; Mohammad Rahim Kadivar; Nastaran Khodadad; Neda Pirbonyeh; Amir Emami
Volume 12, Issue 3 , September 2015, , Pages 198-208
Abstract
Background: A new pandemic influenza A (H1N1) emerged in April 2009, causing considerable morbidity and mortality. Since mutations in the haemagglutinin (HA) may influence the antigenicity and pathogenicity of the virus, continued epidemiological and molecular characterization for the effective control ...
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Background: A new pandemic influenza A (H1N1) emerged in April 2009, causing considerable morbidity and mortality. Since mutations in the haemagglutinin (HA) may influence the antigenicity and pathogenicity of the virus, continued epidemiological and molecular characterization for the effective control of pandemic flu and developing of more appropriate vaccine is crucial. Objective: To monitor the molecular evolution of A (H1N1) pdm09 viruses in a specific time period in Shiraz, Southern Iran. Methods: A total of 200 samples were collected from February-April 2013. HA gene of the isolates was amplified and sequenced. Phylogenetic analysis of the HA gene was performed. Results: Out of 200 samples, a total of 77 (38.5%) samples were confirmed as A (H1N1) pdm09 virus using Real-time PCR method. Nucleotide similarity of our study strains with respect to reference strain A/California/07/2009 (H1N1) was 97.5%-98.5%. Phylogenetic analysis of our study strains indicated that the dominant A (H1N1) pdm09 clade was clade 7 and the dominant genetic group in circulating strains in Shiraz was genetic group 6. Some of our study strains showed substitutions at or in the vicinity of the antigenic sites of the HA1 region which may affect the efficacy of the vaccine. Conclusion: Our study strains showed a high homology to the vaccine strain. Our findings confirm the genetic variability of influenza A (H1N1) pdm09 and highlight the necessity of continuous molecular study of the virus for effective management of influenza.
Mohammad Motamedifar; Jamal Sarvari; Azin Ebrahimpour; Amir Emami
Volume 12, Issue 1 , March 2015, , Pages 27-34
Abstract
Background: Herpes simplex viruses (HSV) are human pathogens that establish lytic and latent infections. Reactivation from latency occurs intermittently, which represents a life-long source for recurrent infection. The role of immune factors in the control of recurrent symptomatic HSV lesions is complex ...
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Background: Herpes simplex viruses (HSV) are human pathogens that establish lytic and latent infections. Reactivation from latency occurs intermittently, which represents a life-long source for recurrent infection. The role of immune factors in the control of recurrent symptomatic HSV lesions is complex and the exact role of cytokines remains unclear. Objective: To assess the levels of tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) along with anti-herpetic IgG and IgM, in the symptomatic reactivation of HSV infection. Methods: Thirty-six patients with recurrent symptomatic herpes infection were selected as the study group and thirty-two healthy individuals with no history of symptomatic labial herpes infection enrolled as the control group. Skin swabs were obtained from lip and skin lesions for viral culture. Confirmation of HSV cytopathic effect was carried out using PCR assay. The levels of TNF-α, IL-10, IgG and IgM were measured using ELISA. Results: The level of TNF-α was significantly lower in individuals with recurrent symptomatic herpes infection in comparison with the controls (p=0.04). Also a significant elevation was observed in the levels of specific IgG in patients compared to controls (p<0.05). Conclusion: The decreased level of TNF-α and increased levels of IgG in individuals with a history of symptomatic reactivation of HSV infection is suggestive of a probable shift in favor of the Th2 immune response.