Search

H5 highly pathogenic avian influenza viruses (HPAIVs) of the A/goose/Guangdong/1/1996 lineage have diversified into multiple clades, threatening wild birds and poultry worldwide. Clade 2.3.4.4b HPAIVs have been consistently isolated in [...]

Since their emergence in [approximately equal to] 2010-11 in China (1), highly pathogenic avian influenza viruses (HPAIVs) that have the hemagglutinin (HA) genes of the H5 subtype classified into the [...]

Ocular herpes, caused by herpes simplex virus type 1 (HSV‐1) and type 2 (HSV‐2) infections, remains an important corneal disease, which may result in loss of vision. Because the frequency of acyclovir resistance in HSV has increased, novel antiviral agents are needed for therapeutic approaches to ocular herpes. Several studies have demonstrated that fusion proteins containing entire ectodomain of HSV glycoprotein D receptors, including herpesvirus entry mediator A (HVEM), nectin‐1 and nectin‐2, and the Fc portion of human IgG (HVEMIg, nectin‐1Ig, and nectin‐2Ig, respectively), can exert antiviral effects in vitro and in vivo. Here, to evaluate the antiviral potential of HVEMIg, nectin‐1Ig, and nectin‐2Ig against ocular infections with HSV, transgenic mice expressing these fusion proteins were ocularly inoculated with HSV‐1 and HSV‐2. Transgenic mouse lines expressing HVEMIg and nectin‐1Ig showed marked resistance to ocular herpes; on the other hand, mouse lines expressing nectin‐2Ig did not. Furthermore, to investigate the therapeutic effects of nectin‐1Ig, which can neutralize HSVs in vitro against ocular disease, transgenic mouse serum containing nectin‐1Ig was dropped into the eyes of wild‐type mice after HSV infection. Reduction of severe symptoms could be observed in mice treated with nectin‐1Ig serum. These results warrant further study of soluble HVEM and nectin‐1 products as preventive and therapeutic agents against ocular herpes caused by HSV‐1 and HSV‐2 infections, especially nectin‐1Ig as a new eye drop. Highlights: Soluble forms of nectin‐1 and HVEM show marked resistance to ocular HSV infection in vivo.Treatment with soluble nectin‐1 is effective in reducing ocular HSV disease. [ABSTRACT FROM AUTHOR]

The article presents a study which explores the creation of reverse transcription-loop-mediated isothermal amplification (RT-LAMP) assay for detecting avian influenza viruses in field samples. The assay is a gene amplification approach for the immediate diagnosis of different infectious diseases. For the study, researchers created specific primers which target the matrix gene in order to observe avian influenza viruses. They collected 34 virus field samples in order to validate the primers. They found that all samples were positive for avian influenza viruses.

The recent epidemic caused by H5N1 highly pathogenic avian influenza (HPAI) viruses has spread over many parts of Asia, Europe and Africa. Wild birds, particularly waterfowl, are considered to play a role in viral dissemination. However, detailed information on whether wild terrestrial birds act as carriers is currently unavailable. To investigate the susceptibility of terrestrial birds to HPAI viruses, two species of wild bird (great reed warbler and pale thrush) that are common in East Asia were infected with H5N1 HPAI virus. The results showed that both species were highly susceptible to the virus. The great reed warbler showed fatal infection with 100% mortality, but the pale thrush survived for longer periods (>8 days) with viral shedding. These findings suggest that there is variation in clinical outcome after infection of wild terrestrial birds, and that some bird species could become subclinical excretors of the H5N1 virus. [ABSTRACT FROM AUTHOR]

Although the US3 gene product of herpes simplex virus (HSV) has been identified as a serine/threonine protein kinase (PK), the functions are poorly understood. We found that US3 PK of HSV-2 induced disruption of actin filaments, cell rounding and accumulation of binucleate cells in HEp2 cells. Cell rounding was abrogated by expression of either kinase-dead forms of US3 PK or a mutant protein lacking the acidic cluster in the kinase regulatory domain. Co‐expression of dominant active forms of Cdc42/Rac inhibited cell rounding, suggesting that a signal transduction pathway involving Cdc42/Rac may play a role in the morphological changes induced by the kinase. Cdc42 and Rac, members of the Rho family of small GTPases, function as molecular switches changing actin cytoskeletal organization, influencing transcription and controlling apoptotic cell death. By computed homology search, we noticed significant similarities between US3 PK and p21-activated kinase (PAK), which is activated by the Cdc42 or Rac. We also found that the expression of US3 suppressed the activation of c-Jun N-terminal kinase (JNK), a kinase that is downstream of PAK. These observations suggest that the US3 PK affects the Cdc42/Rac pathway and can act as an upstream suppressor of JNK in the stress-activated signalling pathway. [ABSTRACT FROM AUTHOR]

Abstract: H5N1 highly pathogenic avian influenza (HPAI) viruses were isolated from dead wild waterfowl at Khunt, Erkhel, Doityn Tsagaan, Doroo, and Ganga Lakes in Mongolia in July 2005, May 2006, May 2009, July 2009, and May 2010, respectively. The isolates in 2005 and 2006 were classified into genetic clade 2.2, and those in 2009 and 2010 into clade 2.3.2. A/whooper swan/Mongolia/6/2009 (H5N1) experimentally infected ducks and replicated systemically with higher mortality than that of the isolates in 2005 and 2006. Intensive surveillance of avian influenza in migratory waterfowl flying from their nesting lakes in Siberia to Mongolia in every autumn indicate that HPAI viruses have not perpetuated at their nesting lakes until 2009. The present results demonstrate that wild waterfowl were sporadically infected with H5N1 HPAI viruses prevailing in domestic poultry in the southern Asia and died in Mongolia on the way back to their northern territory in spring. [Copyright &y& Elsevier]

Previously, we established HEp2 cell lines which express the US3 protein kinase of herpes simplex virus type 2 upon induction with IPTG. Using these cells, we examined whether expression of US3 is sufficient to protect cells from apoptotic cell death induced by sorbitol. Cells expressing US3 showed significantly reduced nuclear fragmentation in the degree that DNA fragmentation and caspase-3 activation were suppressed. It is known that stressors such as osmotic shock and UV irradiation induce the activation of the JNK (c-Jun N-terminal kinase), which can lead to apoptotic cell death. Expression of US3 resulted in the suppression of sorbitol-induced phosphorylation of JNK and MKK4/SEK1, suggesting that the suppression of apoptotic cell death was due to the attenuation of JNK activity. [Copyright &y& Elsevier]