Persistent Shedding of West Nile Virus in Urine of Experimentally Infected Hamsters

Tonry, Jessica H.; Xiao, Shu Yuan; Siirin, Marina; Chen, Hongli; Rosa, A.P.A. Travassos da; Tesh, Robert B.

doi:10.4269/ajtmh.2005.72.320

Cited by 97 publications

(90 citation statements)

References 31 publications

(54 reference statements)

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“…Taken together, the results obtained for ROCV here and those reported in other studies for different flaviviruses , Tonry et al 2005, Siirin et al 2007 suggest that a variety of flaviviruses cause persistent infections in vertebrates and that the persistence of these viruses is not a rare phenomenon. However, further studies are needed to determine exactly how a persistent ROCV infection is established, including the route by which the virus enters the CNS, the cells that permit infection of the CNS and the cell groups involved in the production of virus and in the protective immune response, as well as other aspects of pathogenesis.…”

Section: Discussionsupporting

confidence: 73%

“…Indeed, in an experimental study, Siirin et al (2007) demonstrated that adult hamsters infected with Saint Louis encephalitis virus continued to excrete the virus in urine for a prolonged period of time despite a robust immune response. These findings were similar to those reported for chronic infections with West Nile virus , Tonry et al 2005.…”

supporting

confidence: 81%

“…Urine has been shown to be a good clinical specimen for the isolation of flaviviruses and to demonstrate viral persistence in direct cultures of Vero cells , Tonry et al 2005, Siirin et al 2007. In the present experiment, the virus was isolated from urine, demon- strating that the urine of infected animals is infectious.…”

Section: Discussionmentioning

confidence: 78%

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Persistence of experimental Rocio virus infection in the golden hamster (Mesocricetus auratus)

Henriques

Quaresma

Fuzii

et al. 2012

Mem. Inst. Oswaldo Cruz

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Rocio virus (ROCV) is an encephalitic flavivirus endemic to Brazil. Experimental flavivirus infections have previously demonstrated a persistent infection and, in this study, we investigated the persistence of ROCV infection in golden hamsters (Mesocricetus auratus The viral titres were quantified by real-time-polymerase chain reaction (qRT-PCR). The specimens were used to infect Vero cells and ROCV antigens in the cells were detected by immunefluorescence assay. The levels of antibodies were determined by the haemagglutination inhibition technique. A histopathological examination was performed on the tissues by staining with haematoxylin-eosin and detecting viral antigens by immunohistochemistry (IHC). ROCV induced a strong immune response and was pathogenic in hamsters through neuroinvasion. ROCV was recovered from Vero cells exposed to samples from the viscera, brain, blood, serum and urine and was detected by qRT-PCR in the brain, liver and blood for three months after infection. ROCV induced histopathological changes and the expression of viral antigens, which were detected by IHC in the liver, kidney, lung and brain up to four months after infection. These findings show that ROCV is pathogenic to golden hamsters and has the capacity to cause persistent infection in animals after intraperitoneal infection.

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Section: Discussionsupporting

confidence: 73%

supporting

confidence: 81%

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Persistence of experimental Rocio virus infection in the golden hamster (Mesocricetus auratus)

Henriques

Quaresma

Fuzii

et al. 2012

Mem. Inst. Oswaldo Cruz

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“…In contrast to neurons and macrophages, these latter cells do not die following infection. Instead they survive and often become persistently infected (21,22,29). Consistent with these results, we show that in vitro infection of macrophages with either Dengue-2 or Modoc virus results in cell killing similar to that of CPT at 48 hpi, whereas infection with either virus fails to kill renal epithelial cells and fibroblasts (MDCK, 293T, Vero, SW primary MEF, and C57/Bl primary MEF) even when the cells are infected at extremely high titer (m.o.i.…”

Section: Discussionmentioning

confidence: 99%

Flavivirus NS4A-induced Autophagy Protects Cells against Death and Enhances Virus Replication

McLean

Wudzinska

Datan

et al. 2011

Journal of Biological Chemistry

230

223

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Over 2.5 billion people live in areas at high risk for Dengue and related flavivirus infections (1). Dengue hemorrhagic fever, a severe complication present in ϳ5% of cases, claims more lives annually than all other hemorrhagic fevers combined (2); much of the damage is caused by death of infected cells. The fate of infected cells depends on cell type. Although flavivirus induces apoptosis of neurons and macrophages, infected hepatocytes and epithelial cells do not die. We find that flavivirus up-regulates autophagy in MDCK 3 renal epithelial cells and other cell types and subsequently protects them. We further identify nonstructural protein NS4A of both Dengue-2 and Modoc viruses as the sole viral mediator of autophagy up-regulation and protection against death. Up-regulation of autophagosomes by either live virus infection or NS4A expression depends on PI3K and is important for replication of flavivirus in renal epithelial cells. Flaviviruses often persist in liver and kidney following the acute phase of infection, suggesting that infected cells evade destruction by the host immune response, likely by flavivirusinduced up-regulation of autophagy in these cells. In vitro infection of hepatocytes and fibroblasts leads to up-regulation in autophagy and protection against death (3, 4). More relevant, Dengue-2 viruses replicate within the hepatocyte autophagosomes (5), and inhibition of autophagy attenuates virus replication (3). We extend these findings by identifying the nonstructural viral protein NS4A as the virus-encoded protein that up-regulates autophagy and thus protects the host cell against death, providing a well protected host cell for long term replication of virus.The flavivirus genome contains 10 genes encoding an ϳ11-kDa polyprotein precursor that binds to the ER membrane after translation at the rough ER as follows: three structural proteins (capsid (core) protein, pre-membrane protein ,and envelope glycoprotein) and seven nonstructural genes (NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5) that mediate viral replication, assembly, and evasion of the host immune system. The active proteins are cleaved from the ER-bound viral polyprotein by cellular proteases signalase and furin and viral protease NS3/ 2B. NS3 is both a viral protease (with required cofactor NS2B (6)) and a viral ATP-dependent helicase (7, 8); NS5 is an RNAdependent RNA polymerase and methyltransferase (9) responsible for virus genome replication, whereas NS1 is possibly a part of the viral replication complex (10). The small hydrophobic flavivirus proteins (NS2A, NS4A, and NS4B) remain the most poorly characterized. NS2A is required for the assembly of new flavivirus virions; NS4A associates with the virus replication complex and induces ER membrane rearrangements (discussed below), and NS4B is an antagonist of interferon. Flavivirus NS4A is an ϳ16-kDa membrane-associated protein consisting of four transmembrane helices and an N-terminal cytosolic region. Once the viral genome is translated in the ER,

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“…Because WNV is a neurotropic virus, its pathology in the CNS has been the focus of many studies; therefore, little is known about WNV pathogenesis in organs other than the CNS. Studies of WNV in birds, dogs, and rodents have shown that the kidney is a site of replication (7)(8)(9); moreover, infectious WNV has been recovered from urine samples from experimentally infected hamsters as early as day 1 to day 52 postinfection (9). The purpose of this study was to determine whether WNV is similarly shed in the urine of humans with WNV infections.…”

mentioning

confidence: 99%

West Nile Virus Detection in Urine

Tonry

Brown²,

Cropp

et al. 2005

Emerg. Infect. Dis.

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Persistent Shedding of West Nile Virus in Urine of Experimentally Infected Hamsters

Cited by 97 publications

References 31 publications

Persistence of experimental Rocio virus infection in the golden hamster (Mesocricetus auratus)

Persistence of experimental Rocio virus infection in the golden hamster (Mesocricetus auratus)

Flavivirus NS4A-induced Autophagy Protects Cells against Death and Enhances Virus Replication

West Nile Virus Detection in Urine

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