Mosquito-infecting virus Espirito Santo virus inhibits replication and spread of dengue virus.

The primary vector of dengue virus (DENV) is Aedes aegypti. The mosquito-infecting virus, Espirito Santo virus (ESV), does not infect Vero (mammalian) cells and grows in mosquito (C6/36) cells without cytopathic effects. Effects of ESV infection on replication of DENV were explored in vitro and in vivo, analyzing protein, RNA genome expression, and plaque formation. ESV and DENV simultaneous coinfection did not block protein synthesis from either virus but did result in inhibition of DENV replication in mosquito cells. Furthermore, ESV superinfected with DENV resulted in inhibition of DENV replication and spread in A. aegypti, thus reducing vector competence. Tissue culture experiments on viral kinetics of ESV and DENV coinfection showed that neither virus significantly affects the replication of the other in Vero, HeLa, or HEK cells. Hence, ESV blocks DENV replication in insect cells, but not the mammalian cells evaluated here. Our study provides new insights into ESV-induced suppression of DENV, a globally important pathogen impacting public health.

Detection, infection dynamics and small RNA response against Culex Y virus in mosquito-derived cells.

Many insect cell lines are persistently infected with insect-specific viruses (ISV) often unrecognized by the scientific community. Considering recent findings showing the possibility of interference between arbovirus and ISV infections, it is important to pay attention to ISV-infected cell lines. One example is the Entomobirnavirus, Culex Y virus (CYV). Here we describe the detection of CYV using a combination of small RNA sequencing, electron microscopy and PCR in mosquito cell lines Aag2, U4.4 and C7-10. We found CYV-specific small RNAs in all three cell lines. Interestingly, the magnitude of the detected viral RNA genome is variable among cell passages and leads to irregular detection via electron microscopy. Gaining insights into the presence of persistent ISV infection in commonly used mosquito cells and their interactions with the host immune system is beneficial for evaluating the outcome of co-infections with arboviruses of public health concern.

Structural insights into the multifunctional protein VP3 of birnaviruses.

Infectious bursal disease virus (IBDV), a member of the Birnaviridae family, is the causative agent of one of the most harmful poultry diseases. The IBDV genome encodes five mature proteins; of these, the multifunctional protein VP3 plays an essential role in virus morphogenesis. This protein, which interacts with the structural protein VP2, with the double-stranded RNA genome, and with the virus-encoded, RNA-dependent RNA polymerase, VP1, is involved not only in the formation of the viral capsid, but also in the recruitment of VP1 into the capsid and in the encapsidation of the viral genome. Here, we report the X-ray structure of the central region of VP3, residues 92-220, consisting of two alpha-helical domains connected by a long and flexible hinge that are organized as a dimer. Unexpectedly, the overall fold of the second VP3 domain shows significant structural similarities with different transcription regulation factors.

Attachment and entry of infectious pancreatic necrosis virus (IPNV) into CHSE-214 cells.

Infectious pancreatic necrosis virus (IPNV) attaches to CHSE-214 cells through two types of cell components: specific and non-specific ones. Competition experiments with inactivated IPNV showed that IPNV requires specific components to productively infect cells. Just a low amount of adsorbed IPNV enters the cell. After 20 minutes, part of the adsorbed IPNV was internalized into acid compartments. Also, the viruses adsorbed on the cell surface require similar periods of time to escape from the neutralization of antibodies.

Viruses associated with the epizootic ulcerative syndrome (EUS) of fish in South-East Asia.

A number of birnaviruses, rhabdoviruses and a reovirus have been isolated from occasional fish affected with the epizootic ulcerative syndrome (EUS) in the past decade. The heterogeneous nature of these isolates, together with a low and inconsistent level of recovery from diseases specimens, suggests that these viruses may only represent adventitious infections unrelated to outbreaks of EUS. Furthermore, experimental induction of the condition by direct exposure to cell culture isolated viruses has not been achieved. The significance, if any, of C-type retroviruses identified in cell cultures derived from EUS-susceptible fish species is not known.