The recent explosive outbreak of Zika virus (ZIKV) infection has been reported in South and Central America and the Caribbean. Neonatal microcephaly associated with ZIKV infection has already caused a public health emergency of international concern. No specific vaccines or drugs are currently available to treat ZIKV infection. The ZIKV helicase, which plays a pivotal role in viral RNA replication, is an attractive target for therapy.

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The objective of the study was to extend a nation-wide rotavirus surveillance network in India, and to generate geographically representative data on rotaviral disease burden and prevalent strains.

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Ebola and other filoviruses pose significant public health and conservation threats by causing high mortality in primates, including humans. Preventing future outbreaks of ebolavirus depends on identifying wildlife reservoirs, but extraordinarily high biodiversity of potential hosts in temporally dynamic environments of equatorial Africa contributes to sporadic, unpredictable outbreaks that have hampered efforts to identify wild reservoirs for nearly 40 years.

Ebola and Marburg filovirus disease outbreaks have typically occurred as isolated events, confined to central Africa.

Zika virus is a member of the flavivirus genus that had not been associated with severe disease in humans until the recent outbreaks, when it was linked to microcephaly in newborns in Brazil and to Guillain-Barré syndrome in adults in French Polynesia.

A detailed understanding of serological immune responses to Ebola and Marburg virus infections will facilitate the development of effective diagnostic methods, therapeutics and vaccines. We examined antibodies from Ebola or Marburg survivors 1-14 years after recovery from disease, by using a microarray that displayed recombinant nucleoprotein (NP), viral protein 40 (VP40), envelope glycoprotein (GP), and inactivated whole virions from six species of filoviruses.

Rift Valley fever (RVF) outbreaks have occurred across eastern Africa from 1912 to 2010 approximately every 4–15 years, most of which have not been accompanied by significant epidemics in human populations. However, human epidemics during RVF outbreaks in eastern Africa have involved 478 deaths in 1998, 1107 reported cases with 350 deaths from 2006 to 2007 and 1174 cases with 241 deaths in 2008. We review the history of RVF outbreaks in eastern Africa to identify the epidemiological factors that could have influenced its increasing severity in humans.

Researchers have identified key genes behind the infectivity of a virus that causes hand, foot, and mouth disease. Humans are the only known mammalian host, but in 2014, strains were bred that were capable of infecting mice and primate cell lines. These strains had mutant versions of the virus coat proteins. In this study, the same research group, led by Kaw Bing Chua and Vincent Chow at the National University of Singapore, introduced the mutations into the non-infectious strain individually and in combinations.

The flaviviruses dengue virus (DENV) and Zika virus (ZIKV) are severe health threats with rapidly expanding ranges. To identify the host cell dependencies of DENV and ZIKV, we completed orthologous functional genomic screens using RNAi and CRISPR/ Cas9 approaches. The screens recovered the ZIKV entry factor AXL as well as multiple host factors involved in endocytosis (RAB5C and RABGEF), heparin sulfation (NDST1 and EXT1), and transmembrane protein processing and maturation, including the endoplasmic reticulum membrane complex (EMC).

The human disease Japanese encephalitis (JE) can be prevented by vaccination, although it is not entirely clear if the emerging JEV G5 genotype can be controlled using the vaccine based on the G3 genotype. Consequently, we systematically compared G3 and G5 cross-neutralizing immune responses in vaccinated humans and, separately, cross-protective immune responses in mice using the current G3 JE vaccine to induce the immunity.