by J Hyg Epidemiol Microbiol Immunol. of anti-WNV IgM and immunoglobulin G (IgG) was 7.1% (95% confidence interval [CI], 5.9 to 8.3) and 76.5% (95% CI, 74.0 to 78.8), respectively. The WNV RNA prevalence was 1.9% (95% CI, 1.4 to 2.9), while 14.3% (95% CI, 12.9 to 15.8) had WNV-neutralizing antibodies. In animals, the pooled seroprevalence of anti-WNV IgM and IgG was 90.3% (95% CI, 84.3 to 94.6) and 3.5% (95% CI, 1.9 to 5.8), respectively, while 20.0% (95% CI, 12.9 to 21.4) had WNV-neutralizing antibodies. Age (odds ratio [OR], 3.73; Timegadine 95% CI, 1.87 to 7.45; p<0.001) and level of education (no formal education: OR, 4.31; 95% CI, 1.08 to 17.2; p<0.05; main: OR, 7.29; 95% CI, 1.80 to 29.6; p<0.01) were significant risk factors for Timegadine WNV IgM seropositivity in humans. CONCLUSIONS The findings of this study spotlight the endemicity of WNV in animals and humans in Nigeria and underscore the need for the One Health prevention and control approach. family [2]. In nature, WNV is usually managed in a zoonotic transmission cycle between birds and mosquitos, mainly species. Susceptibility to WNV contamination has also been indicated for many other vertebrate hosts, including reptiles, amphibians, and mammals [3]. Ecologically, horses and humans are dead-end hosts that do not play a role in the transmission cycle of WNV [3]. However, they can manifest severe disease or death as a consequence Goat polyclonal to IgG (H+L)(HRPO) of WNV contamination [3]. Approximately 80% of WNV infections in humans are inapparent, while in other persons, WNV produces flu-like malaise and severe neuroinvasive disorders that currently have no specific cure [4]. Fewer than 1% of WNV-infected persons develop severe WNV disease [4]. The severity of disease in this latter group of individuals is influenced by age, immune status, and terminal comorbidities [4]. The nonneurotropic form of WNV infection can either be mild or critical, with an incubation period of 3-14 days. It is usually accompanied by pyrexia, anorexia, body aches, swollen lymph nodes, and muscle and joint pains [4]. Although the pathogenesis of WNV infections has yet to be completely elucidated, certain studies have revealed the involvement of the hosts genetic factors as a predisposing factor for severe WNV disease [5,6]. Since the first discovery of the virus in 1937 in the West Nile district of Uganda [6], it has undergone significant geographical spread around the world through activities such as globalization, land use, and international travel. WNV infection was first identified in Nigeria in the 1950s [4,7]. Since then, infection with the virus has been reported in many parts of Nigeria and subsequently Timegadine in several other countries across the sub-Saharan African region [7]. Nigeria is a nation in West Africa situated at a latitude of 9.0820N and a longitude of 8.6753E. It shares land borders with the Republic of Benin in the west, Chad and Cameroon in the east, and Niger in the north-east and north-west zones of Nigeria. The southern part of Nigeria is characterized by a tropical rainstorm climate, which is affected by storms that originate from the south Atlantic Ocean and move towards the southwest of Nigeria. Its warmth and high humidity give it a substantial propensity to rise and create abundant rainfall [8]. The tropical monsoon climate has temperature ranges that are consistent throughout the year [8]. The southern part of the country encounters overwhelming and abundant rainfall [8]. The total annual rainfall received in this region is high, above the 2 2,000 mm rainfall threshold that defines the tropical rainforest climate, which is characterized by significant forest cover. However, more than 4,000 mm of rain can be observed in the South South geopolitical zone of Nigeria (Figure 1). Open in a separate window Figure 1. Geopolitical zones of Nigeria, their corresponding elevations above sea level, and pooled West Nile virus (WNV) immunoglobulin M (IgM).
