First Isolation of<i>West Nile virus</i>from a Patient with Encephalitis in the United States

Huang, Cinnia; Slater, Brett; Rudd, Robert J.; Parchuri, Nandakishore; Hull, Rene; Dupuis, Michelle; Hindenburg, Alexander

doi:10.3201/eid0812.020532

Cited by 93 publications

(69 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One of the patients who acquired transfusion transmitted West Nile virus infection subsequently died, and donated organs to four transplant recipients, three of whom developed meningoencephalitis (9). Although, these and other case reports have suggested that organ transplant patients may have more severe disease compared to immunocompetent patients, it is only with seroprevalence data that any true estimates regarding rates of asymptomatic and symptomatic disease can be made in this population (9,10,20,21).…”

Section: Discussionmentioning

confidence: 99%

A Seroprevalence Study of West Nile Virus Infection in Solid Organ Transplant Recipients

Kumar

Drebot

Wong

et al. 2004

American Journal of Transplantation

104

View full text Add to dashboard Cite

West Nile virus (WNV) causes severe neurological disease in less than 1% of infections. However, meningoencephalitis may be more common in immunosuppressed transplant patients. In 2002, a WNV outbreak occurred in our region. To determine the spectrum of disease of community acquired WNV infection and assess public health behavior patterns in transplant recipients, we carried out a seroprevalence study. Patients were enrolled from outpatient transplant clinics in October 2002 and sera were screened for WNV. Questionnaires about WNV were provided to patients. Eight hundred sixteen organ transplant patients were enrolled. The seroprevalence of WNV IgM was 2/816 (0.25%; 95% CI 0.03-0.88%). By extrapolation to our entire transplant population of 2360 patients, and using data from hospital-based surveillance, the risk of meningoencephalitis in a transplant patient infected with WNV is estimated to be 40% (95% CI 16-80%). With regards to knowledge and behavior, 56% patients knew of and 47% used at least one protective measure against WNV. Only 33% used insect repellent. The risk of meningoencephalitis in transplant recipients is much higher than in the general population. There is incomplete knowledge and poor rates of compliance amongst patients with regards to WNV prevention.

show abstract

Section: Discussionmentioning

confidence: 99%

A Seroprevalence Study of West Nile Virus Infection in Solid Organ Transplant Recipients

Kumar

Drebot

Wong

et al. 2004

American Journal of Transplantation

104

View full text Add to dashboard Cite

show abstract

“…3 In addition, quantitative RT-PCR demonstrated 1.1 ϫ 10 6 viral RNA copies/ml of CSF in a fatal case of human WNV encephalitis. 8 Given the dearth of information regarding quantitative aspects of natural WNV infection in mammalian hosts, future work is needed to define more clearly the roles of viral load and replication in encephalitic disease.…”

Section: Discussionmentioning

confidence: 99%

Diagnosis of West Nile Virus Infection in Horses

et al. 2004

View full text Add to dashboard Cite

Abstract. The North American West Nile virus (WNV) epizootic, which began in 1999, has caused significant morbidity and mortality in horses. Because experimental infection has failed to consistently produce encephalitis in inoculated horses, investigation of naturally occurring cases was used to optimize strategies for diagnosis of this disease. Although WNV RNA could be detected by reverse transcriptase-polymerase chain reaction (RT-PCR) performed on whole blood collected from both clinically affected horses and unaffected herdmates, the diagnostic sensitivity of this approach was low compared with IgM-capture enzyme-linked immunosorbent assay. In addition, it was observed that 18.5% of herdmates of clinically ill horses seroconverted to WNV yet exhibited no overt clinical signs of WNV encephalitis. West Nile viral RNA was detected in neural tissue of 46 of 64 dead horses that were suspected of having WNV encephalitis. Some of these animals were IgM negative or had not been tested serologically. A primary cause of death other than WNV encephalitis was identified in 15 of the 64 cases, whereas the final diagnosis for 3 of these cases remains unresolved. Quantitative RT-PCR analysis of neural tissue from WNV RNA-positive horses demonstrated that the medulla contained the highest mean concentration of viral RNA and that WNV RNA could be detected in samples extracted from formalin-fixed neural tissue. A comparison of WNV RT-PCR amplification strategies found that nested RT-PCR improved diagnostic sensitivity only slightly over a single round of amplification and that a quantitative (TaqMan) assay had sensitivity and specificity that were equivalent to those of nested amplification.

show abstract

“…Infection of the nervous system is characteristic of the most severe cases of WNV disease, often resulting in death or long-term neurologic sequelae (26). Pathologies associated with extraneural sites of infection have also been reported, including acute renal failure (11,24).…”

mentioning

confidence: 99%

West Nile Virus Capsid Degradation of Claudin Proteins Disrupts Epithelial Barrier Function

Medigeshi

Hirsch

Brien

et al. 2009

J Virol

View full text Add to dashboard Cite

During acute infection, West Nile virus (WNV) has been reported to infect a variety of cell types in various tissues of both experimentally and naturally infected hosts. Virus infects epithelial cells in the skin, kidney, intestine, and testes, although the importance of these findings is unclear. In the current study, we have observed that WNV infection of kidney tubules in mice coincides with the loss of expression of several members of the claudin family. Proteins of this family are often involved in epithelial barrier formation and function. WNV infection of epithelial cells in culture resulted in a decrease in the transepithelial electrical resistance, an increase in the efflux of mannitol across the monolayer, and a loss of intracellular levels of claudin-1 to -4. WNV capsid alone was sufficient for the degradation event, which was mediated through lysosomal proteases. Since epithelial cells are frequent sites of WNV infection, these observations imply a potential mechanism for virus dissemination and extraneural pathogenesis.

show abstract

First Isolation ofWest Nile virusfrom a Patient with Encephalitis in the United States

Cited by 93 publications

References 14 publications

A Seroprevalence Study of West Nile Virus Infection in Solid Organ Transplant Recipients

A Seroprevalence Study of West Nile Virus Infection in Solid Organ Transplant Recipients

Diagnosis of West Nile Virus Infection in Horses

West Nile Virus Capsid Degradation of Claudin Proteins Disrupts Epithelial Barrier Function

Contact Info

Product

Resources

About