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Summary. -currently, a new trend in development of vaccines against influenza with broader spectrum of efficacy is focused on conserved antigens of influenza virus. The hA2 glycopolypeptide (hA2 gp) is one of conserved antigens, potentially suitable as immunogens inducing cross-protection against influenza. We selected two distinct domains of hA2 gp originating from influenza A virus (IAv) of h3 subtype for induction of antiviral immune response: the ectodomain (ehA2) comprising aa 23-185 and the fusion peptide (FP) comprising n-terminal aa 1-38. BAlB/c mice were immunized with three doses of ehA2 and FP, respectively, and subsequently challenged with 2 lD 50 of IAv of homologous (h3) or heterologous (h7) hA subtype. Both peptides induced significant antibody response and protected mice against the lethal infection. The most efficient protection was achieved with ehA2 against homologous virus.Keywords: influenza A virus; cross-protection; hA2 glycopolypeptide; hA2 ectodomain; fusion peptide; mice; vaccine * corresponding author. e-mail: viruevar@savba.sk; phone: +4212-59302427. Abbreviations: A/chicken/Germany/34 (h7n1) virus, rostock strain; A/Miss = A/Mississippi/1/85 (h3n2) virus; A/rostock = avian hA = hemagglutinin; ehA2 = ectodomain of hA2 gp; FA = Freund΄s adjuvant; FP = fusion peptide; hA0 = hA precursor; hA1 = hA1 glycopolypeptide; hA2 = hA2 glycopolypeptide; IAv(s) = influenza A virus(es); MAb = monoclonal antibody; vrnA = viral rnA; p.i. = post infection

Summary. -We have studied the impact of simultaneous infection of mice with murine gammaherpesvirus (MHV) and infl uenza A virus (IAV) on the immune response and pathogenesis of both infections. Aft er a persistent MHV-68 herpesviral infection had been established, the same mice were super-infected with IAV. Individual parameters of MHV infection (viral DNA detection in organs and blood) and numbers of leukocytes in lungs and spleens were determined. With regard to the assumed reactivation of MHV-68 (mainly in lungs, spleen, thymus and peritoneal exudate cells) we focused our attention on the detection of transcripts, typical either for lytic infection (ORF50) and/or for latency (ORF73). Herpesviral DNA was detected in above mentioned organs in several intervals during the acute phase of IAV co-infection, but the expression of monitored transcripts was lower, i.e. it has decreased. Th ough the reason for such limited expression during acute infl uenza superinfection remains unclear, it is unambiguous that lower MHV-68 expression was detected in lungs and peritoneal exudate cells (PECs) from 3 rd to 10 th day aft er co-infection with IAV. Furthermore, our study showed that the ongoing gammaherpesvirus latency in co-infected mice aff ected the number of cytotoxic T-lymphocytes and neutrophils during the acute IAV infection and lowered their deviations from that of non-infected mice. Th erefore, we suppose that co-infection with herpes and infl uenza viruses could be mutually benefi cial for the host by promoting its defense against both viruses.

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