In vitro homotypic and heterotypic interference by defective interfering particles of West Nile virus

Debnath, Nitish C.; Tiernery, R.; Sil, Bijon Kumar; Wills, Mark R.; Barrett, Alan D.T.

doi:10.1099/0022-1317-72-11-2705

Cited by 25 publications

(17 citation statements)

References 24 publications

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“…Cell-specific differences in infectious particle-to-antigen ratios or the content of RNA-containing defective viral particles also could independently affect the induction of innate immune responses. For example, under certain virus propagation conditions, Vero cell-passaged virus has a high particle-to-PFU ratio, presumably because of the presence of large numbers of noninfectious or defective viral particles (7,31); this may have an adjuvant-like effect in stimulating a cytokine response. Alternatively, differences in NS1 content of the virus stocks could also affect immune responses, Ϫ/Ϫ mice that were infected i.c.…”

Section: Discussionmentioning

confidence: 99%

Toll-Like Receptor 3 Has a Protective Role against West Nile Virus Infection

Daffis¹,

Samuel

Suthar

et al. 2008

J Virol

308

291

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Protection against West Nile virus (WNV) infection requires rapid viralRecent studies have begun to delineate the molecular mechanisms that regulate alpha interferon (IFN-␣) and IFN-␤ induction after infection by RNA and DNA viruses (reviewed in references 13, 24, 25, and 57). Pattern recognition receptors (PRR) sense conserved structural microbial elements identified as pathogen-associated molecular patterns. PRR involved in the recognition of RNA viruses can be divided into two classes. Toll-like receptors (TLR) on the cell surface or within endosomes recognize single-and double-stranded RNA and signal through the adaptor molecules MyD88 and TRIF. In comparison, RIG-I and MDA5 helicases recognize single-and double-stranded RNA in the cytosol and signal through the adaptor protein IPS-1 (also known as MAVS, Cardif, and VISA) (reviewed in references 28, 42, and 55). Recognition by viral RNA sensors results in the downstream activation and nuclear translocation of IRF-3 and IRF-7, which transcriptionally activate IFN-␣ and -␤ gene promoters (46).Cell culture experiments defined TLR3 as a PRR that recognizes double-stranded RNA, activates IRF-3 and NF-B transcriptional pathways, and induces type I IFN (2). The role of TLR3 in vivo in protection against viral infections has been less clear (reviewed in references 5, 36, and 58). Experiments in TLR3Ϫ/Ϫ mice infected with lymphocytic choriomeningitis virus, vesicular stomatitis virus, and reovirus failed to show increased mortality or altered viral burden phenotypes (12). In contrast, TLR3 restricts replication, regulates cytokine production, and protects against infection by mouse cytomegalovirus and encephalomyocarditis virus (EMCV) (21, 54). Indeed, a deficiency in TLR3 in humans was identified as a predisposing genetic risk factor for herpes simplex virus (HSV) encephalitis (61) and influenza A virus-induced encephalopathy (23). An adverse role for TLR3 also has been proposed since TLR3 Ϫ/Ϫ mice infected with influenza, punta toro, and vaccinia viruses showed improved survival and decreased production of inflammatory cytokines (19,26,33). Analogously, conflicting results have been observed with respect to the role of TLR3 in inducing IFN after infection with the encephalitic flavivirus West Nile virus (WNV). TLR3 was largely dispensable for WNV recognition and induction of IFN responses in vitro (15, 47), whereas in mice, an absence of TLR3 protected mice from lethal infection (59). TLR3 Ϫ/Ϫ mice infected via intraperitoneal injection with WNV showed decreased systemic tumor necrosis factor alpha (TNF-␣) and interleukin-6 (IL-6) production, blood-brain barrier (BBB) permeability, and infection in the brain.Given this apparent conflict and our previous studies demonstration of an essential role for IRF-3 in controlling WNV infection (6), we reexamined the pathogenesis of virulent WNV infection in TLR3 Ϫ/Ϫ mice. Remarkably, we observed increased susceptibility of TLR3 Ϫ/Ϫ mice to WNV infection. TLR3 had a modest effect on WNV infection in peripheral tissues and was...

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Section: Discussionmentioning

confidence: 99%

Toll-Like Receptor 3 Has a Protective Role against West Nile Virus Infection

Daffis¹,

Samuel

Suthar

et al. 2008

J Virol

308

291

View full text Add to dashboard Cite

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“…29,30 The DIPs can prevent normal virus particles from replicating because of competition for cell resources and receptors, and this phenomenon occurs most prevalently in infection studies using high multiplicity of infection (i.e., high dose). 29,31 In mosquito cell culture, growth of Japanese encephalitis virus is inhibited by DIPs, 30 and this was also a hypothesized reason for decreased dengue virus infection in Aedes aegypti ; 32 however, this has not yet been explored for mosquitoes and WNV. The lower infection rates at the high dose versus low dose may also be caused by a stronger immune response occurring in 2007 colony mosquitoes that could have been triggered by increased viral replication because of the high dose, although this phenomenon has only been studied in mammalian cells and not mosquito cells infected with WNV.…”

Section: Discussionmentioning

confidence: 99%

Environmental and Biological Factors Influencing Culex pipiens quinquefasciatus (Diptera: Culicidae) Vector Competence for West Nile Virus

Richards

Lord

Pesko³

et al. 2010

The American Society of Tropical Medicine and Hygiene

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Interactions between environmental and biological factors affect the vector competence of Culex pipiens quinquefasciatus for West Nile virus. Three age cohorts from two Cx. p. quinquefasciatus colonies were fed blood containing a low- or high-virus dose, and each group was held at two different extrinsic incubation temperatures (EIT) for 13 days. The colonies differed in the way that they responded to the effects of the environment on vector competence. The effects of mosquito age on aspects of vector competence were dependent on the EIT and dose, and they changed depending on the colony. Complex interactions must be considered in laboratory studies of vector competence, because the extent of the genetic and environmental variation controlling vector competence in nature is largely unknown. Differences in the environmental (EIT and dose) and biological (mosquito age and colony) effects from previous studies of Cx. p. quinquefasciatus vector competence for St. Louis encephalitis virus are discussed.

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“…Occasional exceptions have been reported for strains of vesicular stomatitis virus (Prevec & Kang, 1970;Schnitzlein & Reichman, 1976), Semliki Forest virus (Barrett & Dimmock, 1984b) and West Nile virus (Debnath et al, 1991). Homotypic interference probably reflects a requirement for the recognition of control (replication and encapsidation) sequences in the DI genome by replication and virion proteins expressed by infectious virus enzymes (Giachetti & Holland, 1988).…”

Section: Discussionmentioning

confidence: 99%