Virus west nile pdf

Remember me on this computer. Enter the email address you signed up with and we'll email you a reset link. Need an account? Click here to sign up. Download Free PDF. West Nile virus infection in cats: ABCD guidelines on prevention and management Journal of feline medicine and surgery, Fulvio Marsilio. A short summary of this paper. It is an enveloped virus containing a single molecule mammals including humans , reptiles, amphibians of linear, positive-sense, single-stranded RNA.

Several phylogenetic and ticks. It is maintained in a bird—mosquito—bird lineages can be distinguished but most isolates can be assigned to transmission cycle. The most important vectors are lineages 1 and 2. WNV has a broad host range, comprising mainly bird-feeding mosquitos of the Culex genus; birds and mosquitos, but also mammals including humans , reptiles, maintenance and amplification mainly involve amphibians and ticks.

It can cause disease in humans, horses and passerine birds. WNV can cause disease in humans, several species of birds. The severity of disease depends on the horses and several species of birds following neuro virulence of the infecting virus strain. Disease is uncommon in infection of the central nervous system. Although seroprevalence in cats can be high in endemic Epidemiology areas, clinical disease and mortality are rarely WNV was first identified in from the blood of a febrile patient in reported.

If a cat is suspected of clinical signs due the West Nile district of Uganda. Since then, the virus has spread from to an acute WNV infection, symptomatic treatment Africa via migratory birds to other parts of the world including Central is indicated. The European Advisory Board on Cat Diseases ABCD is More than species of birds have been reported to be infected with a body of experts in immunology, vaccinology and clinical WNV, but maintenance and amplification mainly involve passerine feline medicine that issues guidelines on prevention and birds.

Mortality differs between bird species. The guidelines are based on current scientific knowledge of the diseases and High mortality is seen especially in corvids and robins. In other species available vaccines concerned. In these latter species a low-magnitude viraemia develops The latest version of the West Nile virus which is unlikely to be sufficient to again infect mosquitos.

Humans infection in cats guidelines is available at www. The duration of viraemia EBM grades ranged from 3. The level of viraemia Infection occurs mainly through inoculation The ranking system observed in cats might be high enough to infect of virus by a mosquito bite.

Initial target cells for grading the level mosquitos at low efficiency. However, cats are are keratinocytes and skin-resident dendritic of evidence of a not considered to be epidemiologically impor- cells DCs. The target cells of this article is in the spleen and other visceral organs are described on Since feline WNV infection is mostly subclini- thought to be DCs, macrophages and page of this cal, the need for specific diagnostic tests for neutrophils.

Viral replication leads to Special Issue. In humans and horses, a diag- viraemia. The virus enters the central nervous nosis of WNV infection can be established system CNS , resulting in inflammation of through detection of the virus or virus-specific the medulla, brainstem and spinal cord.

Acute infection can be confirmed Similarly to other mammals and birds, cats by detecting virus-specific immunoglobulin M can be infected through mosquito bites, but also antibodies, although antibodies may be absent orally by eating infected small mammals and in the early phase of infection.

A significant probably also birds, as evidenced by serological rise in WNV antibodies in paired acute and studies and experimental infections. Although seroprevalence of WNV infection Virus can be detected by reverse transcrip- in endemic areas can be high, clinical disease tion PCR in blood samples or infected tissues and mortality are rarely reported.

It seems at necropsy. However, viraemia is short-lived that most infections are subclinical in nature. Virus can also be tive meningoencephalitis of unknown origin, detected in tissues by in situ hybridisation positive immunostaining was detected for and immunohistochemistry. WNV antigen in four cats. All rights reserved. All TMA-reactive donors identified in were offered en- Use of sensitive WNV RNA detection assays in donor screen- rollment into a follow-up study, with return visits scheduled at ing has allowed implementation of several approaches to study approximately weekly intervals for the first 4 weeks, followed by these issues.

The first approach, developed by our group, in- monthly visits for up to 3 additional months or until antibody volved use of the incidence-window period model to compre- seroconversion. After the initial phase of increasing for 4 weeks and then monthly for 3 months. Samples from these earlier visits were used to conduct velopment and symptoms have not been well-defined [11—14, quantitative viral load and plasma cytokine and chemokine im- 18 —22].

Furthermore, available data concerning IgM and IgA munoassays; findings are reported elsewhere [24]. All samples persistence are conflicting [18 —22]. WNV RNA screening, enrollment, and follow-up of viremic For all 3 years, all available serial samples from any donor in donors. The 16 donations of detectable neutralizing antibody activity. Plasma specimens were tested for identify the viremic donation.

Table 1. Characteristics of studies involving blood donors infected with West Nile virus, by year of cohort enrollment. TMA, transcription-mediated amplification. The assays were performed according dom i. The independent cell monolayers in accordance with a standardized protocol de- variable was the log-transformed EIA sample-to-calibrator ratio veloped by the Centers for Disease Control and Prevention [28]. Actual donor return times varied, re- curve. The models were fit to the data by use of the R statistical sulting in intermittent collection of blood specimens.

Because package [33]. The median window periods de- conducted with the approval of the Western Investigational Re- fined as the intervals between the selected viral RNA thresholds view Board. All donors gave written informed from an accelerated failure time model [30]. The window period consent for WNV screening and follow-up testing.

For purposes of illustration, the index donation i. These occurred at the midpoint of the window of RNA detectability. The durations of various 6. The mixed-effect models ac- 7. The median time count for the multiple measures per donor by estimating ran- between IgM and IgG seroconversion was 3. The top 3 intervals represent window periods that start with the index donation i. Values are not additive i. RNA was detectable for an additional 6.

See Subjects, Materials, and Methods for a description of window periods. For such donors, the time from the index donation to IgM positivity or IgG positivity was 0 days not interval censored and used in the analysis.

NAT-reactive blood donations [11, 12]. Four 3. In each case, a low Our current data establish that IgM antibody becomes detect- percentage e. The donor tion [7, 11, 12, 21, 22, 24]. IgG develops within 3. Although IgA levels were not directly measured in our on days 57, 83, and after the index donation. A minimum follow-up period RNA for an additional In all cases, this were followed up for the full 12 months. Therefore, if IgM positivity. The viral and antibody dynamics that we report are influenced Our data, combined with previously reported observations, al- by the assays we used.

Our antibody assays could not detect an- low us to formulate a comprehensive picture of the dynamics of tibody in immune complexes, and our RNA assay did not detect viremia and antibody production in persons with WNV infec- cell-associated WNV, which has been demonstrated to occur tion figure 1. The dynamics of the very earliest phase of infec- [38].

To explore these relationships, further studies would be tion, defined as the time from a bite by an infected mosquito to needed. In the current study, we analyzed a data set humans [34 —37]. This level of WNV has been demonstrated to transmit study in order to better fit these expanded data. IgM disappeared infection by the transfusion route, which has led to the imple- before IgA mean times to seroreversion, days for IgM and mentation of targeted ID-NAT donor screening during epidem- days for IgA.

NA, not available; NT, not tested. Each chart represents index ratios measured in untransformed linear scales. Our finding that viremia is present for at least 7 days before development of IgM and persists for 9.

This sug- gests that the sensitivity of the NAT used in the diagnostic labo- ratory expressed by Tilley et al. Further study will be needed to corroborate this hypothesis. These clinical surveillance data have generated the current work- ing hypothesis that viremic units that are also positive for WNV- Figure 3. Fitting of linear mixed models to the log-transformed specific antibody are not infectious when transfused. Second, no docu- immunologic response to WNV infection acquired during the mented transmissions from antibody-positive units occurred previous mosquito season.

Because of the logistics of blood donor testing, it is very diffi- We used our current data on WNV dynamics to estimate the cult to notify and enroll donors within the first several days after number of antibody-positive blood components with low-level a viremic donation.

Given rapid viremia development and sero- viremia i. Our calculation is based on the relative durations of collected at closely spaced intervals immediately after infection, the window periods of MP-NAT positivity 6. ID-NAT detection limit were donated in these 3 years [44]. This 7. Analytical and clinical sensitivity likely would have resulted in the transfusion of WNV- of West Nile virus RNA screening and supplemental assays available in Transfusion ; —9.

New Engl J Med ; — 8. Because all 7 cases of posttransfusion WNV 9. Triggers for switching from infection during — were traced to units that were neg- minipool testing by nucleic acid testing for West Nile virus: analysis of ative for WNV-specific antibody but positive for WNV RNA by data to inform decision making.

Transfusion ; — West Nile virus among blood Because the potential for transmissions from low-level vire- donors in the United States, and N Engl J Med ; —9.

Screening the blood supply for cally powered human transfusion— based look-back studies, the West Nile virus RNA by nucleic acid amplification testing. This recommen- West Nile virus infections pro- jected from blood donor screening data, United States, The cost-effectiveness of adjustment to allow for even longer persistence.

In this report, screening the US blood supply for West Nile virus. Ann Intern Med ; — We found only ; — Centers for Disease Control and Prevention.

West Nile virus transmis- sion—South Dakota, Our estimates therefore sug- Self-reported symptoms associated gest that the day deferral period is a conservative precau- with West Nile virus infection in RNA-positive blood donors. Transfu- tionary policy, particularly because all samples with persistent sion ; —7. Combined with the clinical surveillance data discussed human flaviviral encephalitis infections in the United States.

Clin Diagn above, it is highly unlikely that a blood donation obtained after Lab Immunol ; —9. J Clin Microbiol ; —9. Persistence of virus-reactive serum WNV transmission through transfusion of blood from previ- immunoglobulin M antibody in confirmed West Nile virus encephalitis cases. Emerg Infect Dis ; —9. WNV season in the United States. Clin Diagn Lab Immunol ; — 8.

Development and persistence of West Nile virus immunoglobulin 1. West Nile virus: a primer for the clinician.