West Nile Virus Screening

West Nile virus (WNV), a single-stranded RNA flavivirus, is primarily spread by the mosquito Aedes albopictus. The only screening test used for WNV is nucleic acid testing (NAT), although IgG and IgM antibody testing may be used for donor counseling. Many donors have low viral copy numbers of circulating WNV, which result in false-negative testing by minipool (MP) NAT but can be identified by individual donor (ID) NAT. Thus, during local WNV activity, testing is switched from MP-NAT to ID-NAT.

WNV transmission involves birds and mosquitoes, and thus humans are incidental hosts. In 1999, WNV was first reported in the United States in New York and subsequently spread westward throughout the continental United States where it caused (and still causes) significant seasonal epidemics. While ∼80% of human WNV infections are asymptomatic, symptomatic infections result in fever, muscle ache and headache, nausea, and vomiting. About 1 in 150 infected individuals will have severe disease resulting in meningitis and/or encephalitis (convulsion, coma, paralysis) and, less frequently, death.

Transfusion transmission of WNV was confirmed in 23 patients after RBC, platelet, and plasma transfusions in 2002. Of the 16 donors of these 23 units, 9 had viral symptoms before or after donation and 5 were asymptomatic (2 were lost to follow-up).

In October 2002, the FDA issued guidance on WNV for deferral of donors with suspected or acute WNV infection and for retrieval and quarantine of any blood products from donors with postdonation illness that could be from WNV infection (deferral of donors based on donor questionnaire was retracted in 2005). By summer of 2003, it was recognized that a screening test for WNV was needed and an MP-NAT was implemented. From 2003 to 2005, >1000 viremic donors were documented and seven cases of probable or confirmed transfusion transmission occurred. It became increasingly recognized that many donors had low viral copy numbers of circulating WNV, which result in false-negative testing by MP-NAT but could be identified by ID-NAT. Thus, the testing algorithm was changed from MP testing only to establishing a trigger (and detrigger) for ID-NAT; that is, MP-NAT was used until viremic donations were identified in the geographic area of the donor’s residence, then ID-NAT was used in that geographic area to increase sensitivity. In 2006, at least one case of transfusion-transmitted WNV was reported, resulting in further changes in the testing algorithm, most notably triggering ID-NAT on only one positive donor in the geographic area. This was followed by FDA guidance supporting this scenario. Area of residence could be determined by zip codes, county, or other comparable well-specified regions. These steps have mitigated WNV transfusion transmission.