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Zika virus (ZIKV) has emerged as a major global public health concern in the last two years due to its link as a causative agent of human birth defects. Its rapid expansion into the Western Hemisphere as well as the ability to be transmitted from mother to fetus, through sexual transmission and possibly through blood transfusions has increased the need for a rapid and expansive public health response to this unprecedented epidemic. A non-invasive and rapid ZIKV diagnostic screening assay that can be performed in a clinical setting throughout pregnancy is vital for prenatal care of women living in areas of the world where exposure to the virus is possible. To meet this need we have developed a sensitive and specific reverse transcriptase loop-mediated isothermal amplification (RT-LAMP) assay to detect ZIKV RNA in urine and serum with a simple visual detection. RT-LAMP results were shown to have a limit of detection 10-fold higher than qRT-PCR. As little as 1.2 RNA copies/μl was detected by RT-LAMP from a panel of 178 diagnostic specimens. The assay was shown to be highly specific for ZIKV RNA when tested with diagnostic specimens positive for dengue virus (DENV) and chikungunya virus (CHIKV). The assay described here illustrates the potential for a fast, reliable, sensitive and specific assay for the detection of ZIKV from urine or serum that can be performed in a clinical or field setting with minimal equipment and technological expertise.

Serodiagnosis of arthropod-borne viruses (arboviruses) at the Division of Vector-Borne Diseases, CDC, employs a combination of individual enzyme-linked immunosorbent assays and microsphere immunoassays (MIAs) to test for IgM and IgG, followed by confirmatory plaque-reduction neutralization tests. Based upon the geographic origin of a sample, it may be tested concurrently for multiple arboviruses, which can be a cumbersome task. The advent of multiplexing represents an opportunity to streamline these types of assays; however, because serologic cross-reactivity of the arboviral antigens often confounds results, it is of interest to employ data analysis methods that address this issue. Here, we constructed 13-virus multiplexed IgM and IgG MIAs that included internal and external controls, based upon the Luminex platform. Results from samples tested using these methods were analyzed using 8 different statistical schemes to identify the best way to classify the data. Geographic batteries were also devised to serve as a more practical diagnostic format, and further samples were tested using the abbreviated multiplexes. Comparative error rates for the classification schemes identified a specific boosting method based on logistic regression \"Logitboost\" as the classification method of choice. When the data from all samples tested were combined into one set, error rates from the multiplex IgM and IgG MIAs were <5% for all geographic batteries. This work represents both the most comprehensive, validated multiplexing method for arboviruses to date, and also the most systematic attempt to determine the most useful classification method for use with these types of serologic tests.

In 2002, 23 patients in the United States were confirmed to have acquired the West Nile virus through the transfusion of red cells, platelets, or plasma. Most of these patients were immunocompromised or at least 70 years of age, and meningoencephalitis developed in 13 patients about 10 days after the receipt of the implicated blood product. In 2002, 23 patients acquired the West Nile virus through transfusion. West Nile virus is a mosquito-borne flavivirus that is transmitted primarily among birds; humans serve as incidental hosts. In the United States, human infection with the virus was first recognized in 1999 in Queens, New York. 1 , 2 By 2002, the known geographic range of West Nile virus had expanded to 44 states and the District of Columbia, 3 and that same year, 4200 cases of West Nile virus–associated illness were reported in humans (Centers for Disease Control and Prevention [CDC]: unpublished data). This represents an increase by a factor of nearly 30 over the 149 cases reported in humans from 1999 . . .

Zika virus is a flavivirus known to cause human infection in Asia and Africa. This article describes an outbreak of Zika virus infection on Yap Island, Federated States of Micronesia, with predominant symptoms of rash, fever, arthralgia, and conjunctivitis. An estimated 73% of Yap residents 3 years of age or older became infected during the 4 months of the outbreak. This article describes an outbreak of Zika virus infection on Yap Island, Federated States of Micronesia, with predominant symptoms of rash, fever, arthralgia, and conjunctivitis. An estimated 73% of Yap residents 3 years of age or older became infected. Zika virus is a flavivirus (family Flaviviridae) related to West Nile, dengue, and yellow fever viruses. 1 Zika virus was isolated in 1947 from a rhesus monkey in the Zika forest near Entebbe, Uganda 2 ; its genome was sequenced in 2006. 3 There is serologic evidence of human Zika virus infection in Africa and Asia, and the virus has been isolated from humans in Uganda, Nigeria, and Senegal. 2 – 12 Zika virus is believed to be transmitted to humans by infected mosquitoes and has been isolated from Aedes africanus, Aedes luteocephalus, and Aedes aegypti . 13 – 16 No outbreaks and only 14 cases of . . .

Background. The dynamics of the early stages of West Nile virus (WNV) infection can be assessed by follow-up studies of viremic blood donors. Methods. A total of 245 donors with WNV viremia were followed up weekly for 4 weeks and then monthly for up to 6 additional months or until seroconversion. Plasma samples were tested for WNV RNA by transcription-mediated amplification (TMA) and for WNV-specific IgM and IgG antibodies. RNA persistence was investigated by 6 replicate TMA tests; samples that were viremic for $gt; 40 days were tested for WNV-neutralizing activity. Follow up of 35 additional viremic donors for up to 404 days was conducted to evaluate persistence of WNV-specific antibody. Results. The median time from RNA detection to IgM seroconversion was 3.9 days; to IgG seroconversion, 7.7 days; to RNA negativity by single-replicate TMA, 13.2 days; and to RNA negativity by 6-replicate TMA, 6.1 additional days after results of single-replicate TMA are negative. For 4 donors in whom RNA persisted for > 40 days after the index donation, all samples obtained after this threshold were also positive for WNV IgG and neutralizing activity. The mean times to IgM and IgA negativity were 156 and 220 days, respectively. Conclusions. IgM and IgG develop rapidly after viremia and before RNA levels become undetectable, which occurred a mean of 13.2 days after the index donation among donors in this study. WNV RNA detection by replicate TMA rarely persists for > 40 days after the index donation and is accompanied by WNV-specific neutralizing antibody, consistent with an absence of WNV transmission via transfusion of seropositive blood components.

West Nile (WN) virus is a mosquito-borne flavivirus and human, equine, and avian neuropathogen. The virus is indigenous to Africa, Asia, Europe, and Australia, and has recently caused large epidemics in Romania, Russia, and Israel. Birds are the natural reservoir (amplifying) hosts, and WN virus is maintained in nature in a mosquito-bird-mosquito transmission cycle primarily involving Culex sp mosquitoes. WN virus was recently introduced to North America, where it was first detected in 1999 during an epidemic of meningoencephalitis in New York City. During 1999–2002, the virus extended its range throughout much of the eastern parts of the USA, and its range within the western hemisphere is expected to continue to expand. During 1999–2001, 142 cases of neuroinvasive WN viral disease of the central nervous system (including 18 fatalities), and seven cases of uncomplicated WN fever were reported in the USA. Most human WN viral infections are subclinical but clinical infections can range in severity from uncomplicated WN fever to fatal meningoencephalitis; the incidence of severe neuroinvasive disease and death increase with age. Serology remains the mainstay of laboratory diagnosis. No WN virus-specific treatment or vaccine is available. Prevention depends on organised, sustained vector mosquito control, and public education.

In fall 2017, 3 solid organ transplant (SOT) recipients from a common donor developed encephalitis within 1 week of transplantation, prompting suspicion of transplant-transmitted infection. Eastern equine encephalitis virus (EEEV) infection was identified during testing of endomyocardial tissue from the heart recipient. We reviewed medical records of the organ donor and transplant recipients and tested serum, whole blood, cerebrospinal fluid, and tissue from the donor and recipients for evidence of EEEV infection by multiple assays. We investigated blood transfusion as a possible source of organ donor infection by testing remaining components and serum specimens from blood donors. We reviewed data from the pretransplant organ donor evaluation and local EEEV surveillance. We found laboratory evidence of recent EEEV infection in all organ recipients and the common donor. Serum collected from the organ donor upon hospital admission tested negative, but subsequent samples obtained prior to organ recovery were positive for EEEV RNA. There was no evidence of EEEV infection among donors of the 8 blood products transfused into the organ donor or in products derived from these donations. Veterinary and mosquito surveillance showed recent EEEV activity in counties nearby the organ donor's county of residence. Neuroinvasive EEEV infection directly contributed to the death of 1 organ recipient and likely contributed to death in another. Our investigation demonstrated EEEV transmission through SOT. Mosquito-borne transmission of EEEV to the organ donor was the likely source of infection. Clinicians should be aware of EEEV as a cause of transplant-associated encephalitis.

This investigation documents severe West Nile virus infections in four recipients of organs from a single donor. Three of the recipients had encephalitis. The probable source of infection in the donor was a blood transfusion from a blood donor with West Nile virus viremia. Transmission of the virus by both transplanted organs and transfused blood. West Nile virus infects birds and mosquitoes; humans and horses are incidental hosts. As of April 15, 2003, in the United States, 4156 cases had been reported in 39 states and the District of Columbia (Centers for Disease Control and Prevention [CDC]: unpublished data). Although transmission of West Nile virus through blood or organs has not previously been documented, such transmission has been postulated. 1 The virus may be transiently present in the blood or organs of infected persons, many of whom probably have no symptoms. The widespread epidemic of West Nile virus infections in 2002 in the United States has . . .

West Nile virus (WNV) causes an acute infection that is usually cleared by an effective immune response after several days of viremia. However, a recent study detected WNV RNA in the urine of 5 of 25 persons (20%) tested several years after their initial acute WNV disease. We evaluated an established cohort of 40 persons >6 years after initial infection with WNV. Urine collected from all participants tested negative for WNV RNA by reverse-transcription polymerase chain reaction and transcription-mediated amplification. Prospective studies are needed to determine if and for how long WNV persists in urine following WNV disease.

CDC has developed interim guidelines for health care providers in the United States who are caring for infants born to mothers who traveled to or resided in an area with Zika virus transmission during pregnancy. These guidelines include recommendations for the testing and management of these infants. Guidance is subject to change as more information becomes available; the latest information, including answers to commonly asked questions, can be found online (http://www.cdc.gov/zika). Pediatric health care providers should work closely with obstetric providers to identify infants whose mothers were potentially infected with Zika virus during pregnancy (based on travel to or residence in an area with Zika virus transmission [http://wwwnc.cdc.gov/travel/notices]), and review fetal ultrasounds and maternal testing for Zika virus infection (see Interim Guidelines for Pregnant Women During a Zika Virus Outbreak*) (1). Zika virus testing is recommended for 1) infants with microcephaly or intracranial calcifications born to women who traveled to or resided in an area with Zika virus transmission while pregnant; or 2) infants born to mothers with positive or inconclusive test results for Zika virus infection. For infants with laboratory evidence of a possible congenital Zika virus infection, additional clinical evaluation and follow-up is recommended. Health care providers should contact their state or territorial health department to facilitate testing. As an arboviral disease, Zika virus disease is a nationally notifiable condition.