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West Nile Virus Infection in Ogbomoso: Serological Evidence a
a
Oladipo Elijah Kolawole & Oloke Julius Kola a
Department of Pure and Applied Biology (Microbiology/Virology Unit), Ladoke Akintola University of Technology, Ogbomoso, Nigeria Accepted author version posted online: 25 Feb 2015.Published online: 25 Feb 2015.
Click for updates To cite this article: Oladipo Elijah Kolawole & Oloke Julius Kola (2015) West Nile Virus Infection in Ogbomoso: Serological Evidence, Journal of Immunoassay and Immunochemistry, 36:6, 573-578, DOI: 10.1080/15321819.2015.1017105 To link to this article: http://dx.doi.org/10.1080/15321819.2015.1017105
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms &
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Journal of Immunoassay and Immunochemistry, 36:573–578, 2015 Copyright © Taylor & Francis Group, LLC ISSN: 1532-1819 print/1532-4230 online DOI: 10.1080/15321819.2015.1017105
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WEST NILE VIRUS INFECTION IN OGBOMOSO: SEROLOGICAL EVIDENCE
Oladipo Elijah Kolawole and Oloke Julius Kola Department of Pure and Applied Biology (Microbiology/Virology Unit), Ladoke Akintola University of Technology, Ogbomoso, Nigeria
A seroepidemiological study for West Nile virus was carried out in an urban and rural settlements in Ogbomoso for its IgM and IgG. Human sera was obtained and West Nile virus IgM and IgG was determined using Enzyme Linked Immunosorbent Assay technique. Out of 93 subjects tested, 19.4% and 12.9% were positive for IgG and IgM, respectively. Among the urban dwellers, 23.40% were positive for both IgG and IgM, while the rural dwellers had 15.22% for IgG and 2.17% for IgM. Test for pure antibody to West Nile virus revealed that 23.7% had the virus while 8.6% had antibodies that cross reacted for other flaviviruses. Results show that West Nile virus is circulating in Ogbomoso and its environ which might have accounted for malaria like infection in the region. Keywords West Nile, ELISA, immunoglobulin, ogbomoso, flaviviruses
INTRODUCTION West Nile Virus (WNV) is a mosquito-borne zoonotic arbovirus belonging to the genus Flavivirus in the family Flaviviridae. This flavivirus is found in temperate and tropical regions of the world. It was first identified in the West Nile sub-region in the East African nation of Uganda in 1937,[1] but was not viewed as a potentially important public health threat until it was associated with epidemics of fever and encephalitis in the Middle East in the 1950s.[2] WNV has now spread globally, with the first case in the Western Hemisphere being identified in New York City in 1999.[1] The main mode of WNV transmission is via various species of mosquitoes which are the prime vector, with birds being the most commonly infected animal and serving as the prime reservoir host—especially passerines which are of the largest order (Passeriformes) of birds.[3] Address correspondence to Oladipo Elijah Kolawole, Department of Pure and Applied Biology (Microbiology/Virology Unit), Ladoke Akintola University of Technology, P.M.B. 4000, Ogbomoso, 210214, Nigeria. E-mail: [email protected]
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West Nile virus may also be spread through blood transfusions and organ transplants. It is possible for an infected mother to spread the virus to her child through breast milk.[4] Definitive diagnosis of WNV is obtained through detection of virus-specific IgM and neutralizing antibodies. A positive test for West Nile IgG in the absence of a positive West Nile IgM is indicative of a previous flavavirus infection and is not by itself evidence of an acute West Nile virus infection.[5] Currently, no vaccine or specific antiviral treatment against WNV infection is available. The best method to reduce the rates of WNV infection is mosquito control on the part of municipalities, businesses, and individual citizens. Epidemiological surveillance has been instrumental in characterizing clinical disease presentation and disease outcome, as well as identifying high risk populations and factors associated with serious WNV disease.[6] Epidemiological surveillance has also detected and quantified alternative routes of WNV transmission to humans, such as contaminated blood donations and organ transplantation.[7,8] Therefore, the study was carried out to quantify the intensity of virus transmission in a region in order to provide a predictive index of human infection risk. MATERIALS AND METHODS Study Site Ogbomoso the study site is located in Oyo State, south western region of Nigeria. Its geographical coordinates are 8◦ 8’ 0’’ North, 4◦ 16’ 0’’ East. Blood samples were collected specifically from two settlements in Ogbomoso for effective and a more precise determination of the West Nile virus antibodies. Ayeedaade, an urban settlement in Ogbomoso South Local Government is selected for the determination of the antibodies to analyze the seroprevalence of the virus amidst the urban dwellers, while Otamokun, a rural settlement in Ogo–Oluwa Local Government of Ogbomoso, is selected to determine the seroprevalence of the virus amidst the rural dwellers. Study Population Blood samples were collected from subjects who consented to participate in the study and questionnaires providing information about the subjects’ names, medical history, age, sex, town, and date of sample collection was administered alongside. Sample Collection and Analysis Blood samples were collected from the subjects into plain bottles, using needle and syringe, tourniquet, cotton wool, and methylated spirit. The
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collected blood samples were then spun using a centrifuge at 3000 rpm for 10 min to obtained serum. The blood serum was then collected into the cryovials using a sterile Pasteur pipette and stored at −20◦ C prior to analyzing. The sera were tested for WNV IgM and IgG by the Enzyme-Linked Immunosorbent Assay (ELISA) test. The WNV-specific IgM/IgG antibodies were studied by the commercial WKEA Med Supplies Corp, WNV IgM/ IgG ELISA Kit (China), according to the manufacturer’s instructions. All the specimens were analyzed using the enzyme linked immunoassay test. The presence or absence of WNV IgM/IgG was determined by comparing the sample absorbance with the absorbance of the cut-off calibrator. Statistical Analysis The data obtained were subjected to descriptive statistical analysis using SPSS version 17.0 (SPSS Inc., Chicago, IL, USA). RESULTS In this study, 93 subjects were tested with ages ranging from age 0–75. Table 1 shows seroprevalence of WNV antibodies among the study subjects. Out of the 93 blood sera that was tested for WNV antibodies, 18 (19.4%) tested positive for WNV IgG while 12 (12.9%) tested positive for WNV IgM. The highest prevalence of WNV IgG (42.85%) and WNV IgM (28.57%). was found in the age group 0–15, respectively, while the lowest prevalence of WNV IgG (15%) was found in the age group 46–60 and the lowest prevalence of WNV IgM (8.57) was found in the age group 31–45 (0%), as shown in Table 1. The geographical distribution of WNV antibodies in Ogbomoso environs is shown in Table 2. Out of 47 urban dwellers that were tested, 11 (23.40%) tested positive for WNV IgG and WNV IgM, respectively. Out of the 46 rural dwellers, 7 (15.22%) tested positive for WNV IgG while 1 (2.17%) tested positive for WNV IgM as shown in Table 2. Table 3 shows an overall result presenting the cross reactivity by other flaviviruses using the age range. The highest occurrence of cross reactivity (16.7%) was found within tested subjects in the age range 61–75. Also, the highest prevalence of antiWNV IgG and anti-WNV IgM (71.4%) was observed in the age range of 0–15. Table 4 shows the statistical analysis of variance for cross reactivity of other flaviviruses at different age ranges. Age group 31–45 has a mean value of 6.00 for anti-WNV IgG while age group 46–60 have a mean value of 4.00 for anti-WNV IgM. The table also shows the mean value of cross reactivity which is 4.00 which falls within age group 31–45 and the mean value of pure WNV antibody is 7.00 which falls in the age group 46–60. Considering anti-WNV IgG, age group 0–15 has a mean value of 3.00 which is significantly different to age groups, 16–30 (5.00), 31–45 (6.00), 61–75 (1.00) but not to 46–60
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TABLE 1 Age distribution of West Nile virus antibodies
Age Range
No of Subjects Tested (%)
anti- WNV IgG Positve (%)
anti- WNV IgM Positive (%)
7 (7.5) 25 (26.9) 35 (37.6) 20 (21.5) 6 (6.5) 93 100
3 (42.85) 5 (20) 6 (17.14) 3 (15) 1 (16.67) 18 19.4
2 (28.57) 3 (12) 3 (8.57) 4 (20) − 12 12.9
0–15 16–30 31–45 46–60 61–75 TOTAL (%)
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TABLE 2 Geographical distribution of West Nile virus antibodies Geographical Distribution (%) URBAN RURAL TOTAL (%)
No of subjects tested (%)
anti-WNV IgG Positive (%)
anti-WNV IgM Positive (%)
47 (50.5) 46 (49.5) 93 100
11 (23.40) 7 (15.22) 18 19.4
11 (23.40) 1 (2.17) 12 12.9
TABLE 3 Cross reactivity of other flavivirus using age range
Age Range 0–15 16–30 31–45 46–60 61–75 TOTAL (%)
No of Subjects Tested (%)
anti-WNV IgG (%)
anti-WNV IgM (%)
7 (7.5) 25 (26.9) 35 (37.6) 20 (21.5) 6 (6.5) 93 (100)
3 (42.9) 5 (20.0) 6 (17.1) 3 (15.0) 1 (16.7) 18 (19.4)
2 (28.6) 3 (12.0) 3 (8.6) 4 (20.0) − 12 (12.9)
Cross Reactivity Flavivirus anti-WNV IgG+ & anti-WNV IgM− (%) 1 (14.3) 2 (8.0) 4 (11.4) 1 (16.7) 8 (8.6)
Pure Westnile Antibodies (%)
Total No of anti-WNV IgG & anti-WNV IgM (%)
4 (57.1) 6 (24.0) 5 (14.3) 7 (35.0) − 22 (23.7)
5 (71.4) 8 (32.0) 9 (25.7) 7 (35.0) 1 (16.7) 30 (32.3)
(3.00). Also for anti-WNV IgM, age group 0–15 with the mean value 2.00 is significantly different to the age groups, 16–30 (3.00), 46–60 (4.00), 61–75 (0.00) but not to age group 31–45 (2.00). Considering cross reactivity, age group 0–15 with a mean value of 1.00 is significantly different to age groups, 16–30 (2.00), 31–45 (4.00), 46–60 (0.00) but not to 61–75 (1.00). For pure WNV antibody the age group 0–15 has a mean value of 4.00 is significant with all age groups, which are 16–30 (6.00), 31–45 (5.00), 46–60 (7.00), and 61–75 (0.00) This research showed 8 (8.6%) occurrence of cross reactivity while 22 (23.6%) are pure West Nile virus antibodies.
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West Nile Virus in Ogbomoso TABLE 4 Analysis of variance for cross reactivity of other flavivirus using age range
Age Range 0–15 16–30 31–45 46–60 61–75 TOTAL
Total Number of Subject Tested 7 25 35 20 6 93
anti-WNV IgG
anti-WNV IgM
Cross Reactivity
Pure WNV antibody
Total anti-WNV
3.00±0.01b 5.00±0.00c 6.00±0.00d 3.00±0.01b 1.00±0.00a 36±0.46
2.00±0.00b 3.00±0.01c 2.00±0.00b 4.00±0.02d 0.00±0.00a 2.2±0.35
1.00±0.00b 2.00±0.00c 4.00±0.02d 0.00±0.00a 1.00±0.00b 1.6±0.36
4.00±0.02b 6.00±0.00d 5.00±0.00c 7.00±0.00e 0.00±0.00a 4.40±0.36
5.00±0.00 8.00±0.00 9.00±0.00 7.00±0.00 1.00±0.00 6.07±0.81
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Values are mean ± standard error. Means followed by the same superscripts in the column are not significantly different according to Duncan multiple range test at α ≤ 0.05.
DISCUSSION West Nile fever caused by West Nile virus in mild cases is often taken for malaria, this is because both have the same clinical signs, and hence there is need of an effective diagnosis of the virus. Prevalence of anti-WNV IgM (28.57%) was higher in the age group 0–15 and anti-WNV IgG (42.85%) was higher in the age group 0–15 in this study and this has been able to suggest that children has a greater risk of developing severe infection of the virus. This age group is known for more outdoor activities hereby increasing the rate of mosquito bite which serve as a vector for the virus. The seroprevalence from this study according to age is in contrary with Omilabu et al.,[9] the prevalence did not increase with the age distribution. The prevalence of IgG & IgM was higher among the urban dwellers than the rural dwellers which explain more on the seroprevalence of the WNV. The urban settlements having buildings closely built together, poor ventilation, poor drainage system, and over population density makes the settlement a suitable breeding site for mosquitoes. These findings about urban dwellers agrees with Healy,[10] who reported that the neuroinvasive cases of West Nile virus become concentrated in neighborhoods with high property values and housing density and an increased percentage of houses that were unoccupied. Likewise, rapid urbanization has resulted in tremendous increase in vector density as a result of human activities that promote mosquito breeding.[11] According to Papa et al.,[12] it is common in serologic testing for cross-reactions to occur among flaviviruses such as Dengue virus (DENV) and tick-borne encephalitis virus; this necessitates caution when evaluating serologic results of flaviviral infections. Therefore, this study was able to determine pure West Nile virus antibodies and occurrence of cross reactivity according to DOHMH,[5] that a positive test for West Nile IgG in the absence of a positive West Nile IgM is indicative of a previous flavivirus infection and is not by itself evidence of an acute
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West Nile virus infection. The present seroprevalence study of West Nile virus antibodies in Ogbomoso environs has been able to provide useful information on the seroepidemiology of the virus in Ogbomoso. The study shows an exposure to the areas of the community where epidemiological and environmental surveillance is needed. There is currently no human West Nile vaccine, specific treatment, or method to block the bird–mosquito transmission cycle. Therefore, although potentially costly, effective surveillance and preventive efforts are needed and are likely to be less than the costs associated with responding to major West Nile virus outbreaks. The result of this study showed the seroprevalence of WNV IgG 18(19.4%) is higher than WNV IgM 12(12.9%). People should be educated on personal protective measures that can be taken to greatly reduce the risk of being bitten by infected mosquitoes and the government should implement a more effective epidemiological and environmental surveillance system. REFERENCES 1. Nash. D.; Mostashari, F.; Fine, A. The Outbreak of West Nile Virus Infection in the New York City Area in 1999. N. Engl. J. Med. 2001, 344(24), 1807–1814. 2. Paz, S. The West Nile Virus Outbreak in Israel (2000) from a New Perspective: The Regional Impact of Climate Change. Int. J. Environ. Health Res. 2006, 16(1), 1–13. 3. Steinman, A.; Banet-Noach, C.; Tal, S.; Levi, O.; Simanov, L.; Perk, S.; Malkinson, M.; Shpigel, N. West Nile Virus Infection in Crocodiles. Emerg. Infect. Dis. 2003, 9(7), 887–889. 4. Tyler, K.L.; Pape, J.; Goody, R.J.; Corkill, M. Kleinschmidt-DeMasters, B.K. CSF Findings in 250 Patients with Serologically Confirmed West Nile Virus Meningitis and Encephalitis. Neurology 2006, 66(3), 361–365. 5. Department of Health and Mental Hygiene. DOHMH (2012) Advisory #8: West Nile Virus, New York. 6. Lindsey, N.P.; Staples, J.E.; Lehman, J.A.; Fischer, M. Medical Risk Factors for Severe West Nile Virus Disease, United States, 2008–2010. Am. J. Trop. Med. Hyg . 2012, 87 (1), 179–184. 7. Pealer, L.N.; Marfin, A.A.; Petersen, L.R.; Lanciotti, R.S.; Page, P.L.; Stramer, S.L.; Stobierski, M.G.; Signs, K.; Newman, B.; Kapoor, H.; Goodman, J.L.; Chamberland, M.E. Transmission of West Nile Virus through Blood Transfusion in the United States in 2002. N. Engl. J. Med. 2003, 349(13), 1236–1245. 8. Nett, R.J.; Kuehnert, M.J.; Ison, M.G.; Orlowski, J.P.; Fischer, M.; Staples, J.E. Current Practices and Evaluation of Screening Solid Organ Donors for West Nile Virus. Transpl. Infect. Dis. 2012, 14(3):268–277. 9. Omilabu, S.A.; Olaleye, O.D.; Aina, Y.; Fagbami, A.H. West Nile Complement Fixing Antibodies in Nigeria Domestic Animals and Humans. J. Hyg. Epidemiol. Microbiol. Immunol. 1990, 34(4), 357–363 10. Healy, J.; Reisen, W.K.; Kramer, V.; Barker, C.M. Do Current Surveillance Methods Provide Adequate Warning for Human Infections with West Nile Virus? Proc. Mosq. Control Assoc Calif . 2012, 80, 17–21 11. Monath, T.P.; Dengue: The Risk to Developed and Developing Countries. Proc. Nat. Acad. Sci. USA. 1994, 91, 2395–2400. 12. Papa, A.; Karabaxoglou, D.; Kansouzidou, A. Acute West Nile Virus Neuroinvasive Infections: Cross-Reactivity with Dengue Virus and Tick-Borne Encephalitis Virus. J. Med. Virol. 2011, 83(10), 1861–1865. doi:10.1002/jmv.22180.
Journal of Immunoassay and Immunochemistry Publication details, including instructions for authors and subscription information: http://www.tandfonline.com/loi/ljii20
West Nile Virus Infection in Ogbomoso: Serological Evidence a
a
Oladipo Elijah Kolawole & Oloke Julius Kola a
Department of Pure and Applied Biology (Microbiology/Virology Unit), Ladoke Akintola University of Technology, Ogbomoso, Nigeria Accepted author version posted online: 25 Feb 2015.Published online: 25 Feb 2015.
Click for updates To cite this article: Oladipo Elijah Kolawole & Oloke Julius Kola (2015) West Nile Virus Infection in Ogbomoso: Serological Evidence, Journal of Immunoassay and Immunochemistry, 36:6, 573-578, DOI: 10.1080/15321819.2015.1017105 To link to this article: http://dx.doi.org/10.1080/15321819.2015.1017105
PLEASE SCROLL DOWN FOR ARTICLE Taylor & Francis makes every effort to ensure the accuracy of all the information (the “Content”) contained in the publications on our platform. However, Taylor & Francis, our agents, and our licensors make no representations or warranties whatsoever as to the accuracy, completeness, or suitability for any purpose of the Content. Any opinions and views expressed in this publication are the opinions and views of the authors, and are not the views of or endorsed by Taylor & Francis. The accuracy of the Content should not be relied upon and should be independently verified with primary sources of information. Taylor and Francis shall not be liable for any losses, actions, claims, proceedings, demands, costs, expenses, damages, and other liabilities whatsoever or howsoever caused arising directly or indirectly in connection with, in relation to or arising out of the use of the Content. This article may be used for research, teaching, and private study purposes. Any substantial or systematic reproduction, redistribution, reselling, loan, sub-licensing, systematic supply, or distribution in any form to anyone is expressly forbidden. Terms &
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Journal of Immunoassay and Immunochemistry, 36:573–578, 2015 Copyright © Taylor & Francis Group, LLC ISSN: 1532-1819 print/1532-4230 online DOI: 10.1080/15321819.2015.1017105
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WEST NILE VIRUS INFECTION IN OGBOMOSO: SEROLOGICAL EVIDENCE
Oladipo Elijah Kolawole and Oloke Julius Kola Department of Pure and Applied Biology (Microbiology/Virology Unit), Ladoke Akintola University of Technology, Ogbomoso, Nigeria
A seroepidemiological study for West Nile virus was carried out in an urban and rural settlements in Ogbomoso for its IgM and IgG. Human sera was obtained and West Nile virus IgM and IgG was determined using Enzyme Linked Immunosorbent Assay technique. Out of 93 subjects tested, 19.4% and 12.9% were positive for IgG and IgM, respectively. Among the urban dwellers, 23.40% were positive for both IgG and IgM, while the rural dwellers had 15.22% for IgG and 2.17% for IgM. Test for pure antibody to West Nile virus revealed that 23.7% had the virus while 8.6% had antibodies that cross reacted for other flaviviruses. Results show that West Nile virus is circulating in Ogbomoso and its environ which might have accounted for malaria like infection in the region. Keywords West Nile, ELISA, immunoglobulin, ogbomoso, flaviviruses
INTRODUCTION West Nile Virus (WNV) is a mosquito-borne zoonotic arbovirus belonging to the genus Flavivirus in the family Flaviviridae. This flavivirus is found in temperate and tropical regions of the world. It was first identified in the West Nile sub-region in the East African nation of Uganda in 1937,[1] but was not viewed as a potentially important public health threat until it was associated with epidemics of fever and encephalitis in the Middle East in the 1950s.[2] WNV has now spread globally, with the first case in the Western Hemisphere being identified in New York City in 1999.[1] The main mode of WNV transmission is via various species of mosquitoes which are the prime vector, with birds being the most commonly infected animal and serving as the prime reservoir host—especially passerines which are of the largest order (Passeriformes) of birds.[3] Address correspondence to Oladipo Elijah Kolawole, Department of Pure and Applied Biology (Microbiology/Virology Unit), Ladoke Akintola University of Technology, P.M.B. 4000, Ogbomoso, 210214, Nigeria. E-mail: [email protected]
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West Nile virus may also be spread through blood transfusions and organ transplants. It is possible for an infected mother to spread the virus to her child through breast milk.[4] Definitive diagnosis of WNV is obtained through detection of virus-specific IgM and neutralizing antibodies. A positive test for West Nile IgG in the absence of a positive West Nile IgM is indicative of a previous flavavirus infection and is not by itself evidence of an acute West Nile virus infection.[5] Currently, no vaccine or specific antiviral treatment against WNV infection is available. The best method to reduce the rates of WNV infection is mosquito control on the part of municipalities, businesses, and individual citizens. Epidemiological surveillance has been instrumental in characterizing clinical disease presentation and disease outcome, as well as identifying high risk populations and factors associated with serious WNV disease.[6] Epidemiological surveillance has also detected and quantified alternative routes of WNV transmission to humans, such as contaminated blood donations and organ transplantation.[7,8] Therefore, the study was carried out to quantify the intensity of virus transmission in a region in order to provide a predictive index of human infection risk. MATERIALS AND METHODS Study Site Ogbomoso the study site is located in Oyo State, south western region of Nigeria. Its geographical coordinates are 8◦ 8’ 0’’ North, 4◦ 16’ 0’’ East. Blood samples were collected specifically from two settlements in Ogbomoso for effective and a more precise determination of the West Nile virus antibodies. Ayeedaade, an urban settlement in Ogbomoso South Local Government is selected for the determination of the antibodies to analyze the seroprevalence of the virus amidst the urban dwellers, while Otamokun, a rural settlement in Ogo–Oluwa Local Government of Ogbomoso, is selected to determine the seroprevalence of the virus amidst the rural dwellers. Study Population Blood samples were collected from subjects who consented to participate in the study and questionnaires providing information about the subjects’ names, medical history, age, sex, town, and date of sample collection was administered alongside. Sample Collection and Analysis Blood samples were collected from the subjects into plain bottles, using needle and syringe, tourniquet, cotton wool, and methylated spirit. The
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collected blood samples were then spun using a centrifuge at 3000 rpm for 10 min to obtained serum. The blood serum was then collected into the cryovials using a sterile Pasteur pipette and stored at −20◦ C prior to analyzing. The sera were tested for WNV IgM and IgG by the Enzyme-Linked Immunosorbent Assay (ELISA) test. The WNV-specific IgM/IgG antibodies were studied by the commercial WKEA Med Supplies Corp, WNV IgM/ IgG ELISA Kit (China), according to the manufacturer’s instructions. All the specimens were analyzed using the enzyme linked immunoassay test. The presence or absence of WNV IgM/IgG was determined by comparing the sample absorbance with the absorbance of the cut-off calibrator. Statistical Analysis The data obtained were subjected to descriptive statistical analysis using SPSS version 17.0 (SPSS Inc., Chicago, IL, USA). RESULTS In this study, 93 subjects were tested with ages ranging from age 0–75. Table 1 shows seroprevalence of WNV antibodies among the study subjects. Out of the 93 blood sera that was tested for WNV antibodies, 18 (19.4%) tested positive for WNV IgG while 12 (12.9%) tested positive for WNV IgM. The highest prevalence of WNV IgG (42.85%) and WNV IgM (28.57%). was found in the age group 0–15, respectively, while the lowest prevalence of WNV IgG (15%) was found in the age group 46–60 and the lowest prevalence of WNV IgM (8.57) was found in the age group 31–45 (0%), as shown in Table 1. The geographical distribution of WNV antibodies in Ogbomoso environs is shown in Table 2. Out of 47 urban dwellers that were tested, 11 (23.40%) tested positive for WNV IgG and WNV IgM, respectively. Out of the 46 rural dwellers, 7 (15.22%) tested positive for WNV IgG while 1 (2.17%) tested positive for WNV IgM as shown in Table 2. Table 3 shows an overall result presenting the cross reactivity by other flaviviruses using the age range. The highest occurrence of cross reactivity (16.7%) was found within tested subjects in the age range 61–75. Also, the highest prevalence of antiWNV IgG and anti-WNV IgM (71.4%) was observed in the age range of 0–15. Table 4 shows the statistical analysis of variance for cross reactivity of other flaviviruses at different age ranges. Age group 31–45 has a mean value of 6.00 for anti-WNV IgG while age group 46–60 have a mean value of 4.00 for anti-WNV IgM. The table also shows the mean value of cross reactivity which is 4.00 which falls within age group 31–45 and the mean value of pure WNV antibody is 7.00 which falls in the age group 46–60. Considering anti-WNV IgG, age group 0–15 has a mean value of 3.00 which is significantly different to age groups, 16–30 (5.00), 31–45 (6.00), 61–75 (1.00) but not to 46–60
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TABLE 1 Age distribution of West Nile virus antibodies
Age Range
No of Subjects Tested (%)
anti- WNV IgG Positve (%)
anti- WNV IgM Positive (%)
7 (7.5) 25 (26.9) 35 (37.6) 20 (21.5) 6 (6.5) 93 100
3 (42.85) 5 (20) 6 (17.14) 3 (15) 1 (16.67) 18 19.4
2 (28.57) 3 (12) 3 (8.57) 4 (20) − 12 12.9
0–15 16–30 31–45 46–60 61–75 TOTAL (%)
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TABLE 2 Geographical distribution of West Nile virus antibodies Geographical Distribution (%) URBAN RURAL TOTAL (%)
No of subjects tested (%)
anti-WNV IgG Positive (%)
anti-WNV IgM Positive (%)
47 (50.5) 46 (49.5) 93 100
11 (23.40) 7 (15.22) 18 19.4
11 (23.40) 1 (2.17) 12 12.9
TABLE 3 Cross reactivity of other flavivirus using age range
Age Range 0–15 16–30 31–45 46–60 61–75 TOTAL (%)
No of Subjects Tested (%)
anti-WNV IgG (%)
anti-WNV IgM (%)
7 (7.5) 25 (26.9) 35 (37.6) 20 (21.5) 6 (6.5) 93 (100)
3 (42.9) 5 (20.0) 6 (17.1) 3 (15.0) 1 (16.7) 18 (19.4)
2 (28.6) 3 (12.0) 3 (8.6) 4 (20.0) − 12 (12.9)
Cross Reactivity Flavivirus anti-WNV IgG+ & anti-WNV IgM− (%) 1 (14.3) 2 (8.0) 4 (11.4) 1 (16.7) 8 (8.6)
Pure Westnile Antibodies (%)
Total No of anti-WNV IgG & anti-WNV IgM (%)
4 (57.1) 6 (24.0) 5 (14.3) 7 (35.0) − 22 (23.7)
5 (71.4) 8 (32.0) 9 (25.7) 7 (35.0) 1 (16.7) 30 (32.3)
(3.00). Also for anti-WNV IgM, age group 0–15 with the mean value 2.00 is significantly different to the age groups, 16–30 (3.00), 46–60 (4.00), 61–75 (0.00) but not to age group 31–45 (2.00). Considering cross reactivity, age group 0–15 with a mean value of 1.00 is significantly different to age groups, 16–30 (2.00), 31–45 (4.00), 46–60 (0.00) but not to 61–75 (1.00). For pure WNV antibody the age group 0–15 has a mean value of 4.00 is significant with all age groups, which are 16–30 (6.00), 31–45 (5.00), 46–60 (7.00), and 61–75 (0.00) This research showed 8 (8.6%) occurrence of cross reactivity while 22 (23.6%) are pure West Nile virus antibodies.
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West Nile Virus in Ogbomoso TABLE 4 Analysis of variance for cross reactivity of other flavivirus using age range
Age Range 0–15 16–30 31–45 46–60 61–75 TOTAL
Total Number of Subject Tested 7 25 35 20 6 93
anti-WNV IgG
anti-WNV IgM
Cross Reactivity
Pure WNV antibody
Total anti-WNV
3.00±0.01b 5.00±0.00c 6.00±0.00d 3.00±0.01b 1.00±0.00a 36±0.46
2.00±0.00b 3.00±0.01c 2.00±0.00b 4.00±0.02d 0.00±0.00a 2.2±0.35
1.00±0.00b 2.00±0.00c 4.00±0.02d 0.00±0.00a 1.00±0.00b 1.6±0.36
4.00±0.02b 6.00±0.00d 5.00±0.00c 7.00±0.00e 0.00±0.00a 4.40±0.36
5.00±0.00 8.00±0.00 9.00±0.00 7.00±0.00 1.00±0.00 6.07±0.81
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Values are mean ± standard error. Means followed by the same superscripts in the column are not significantly different according to Duncan multiple range test at α ≤ 0.05.
DISCUSSION West Nile fever caused by West Nile virus in mild cases is often taken for malaria, this is because both have the same clinical signs, and hence there is need of an effective diagnosis of the virus. Prevalence of anti-WNV IgM (28.57%) was higher in the age group 0–15 and anti-WNV IgG (42.85%) was higher in the age group 0–15 in this study and this has been able to suggest that children has a greater risk of developing severe infection of the virus. This age group is known for more outdoor activities hereby increasing the rate of mosquito bite which serve as a vector for the virus. The seroprevalence from this study according to age is in contrary with Omilabu et al.,[9] the prevalence did not increase with the age distribution. The prevalence of IgG & IgM was higher among the urban dwellers than the rural dwellers which explain more on the seroprevalence of the WNV. The urban settlements having buildings closely built together, poor ventilation, poor drainage system, and over population density makes the settlement a suitable breeding site for mosquitoes. These findings about urban dwellers agrees with Healy,[10] who reported that the neuroinvasive cases of West Nile virus become concentrated in neighborhoods with high property values and housing density and an increased percentage of houses that were unoccupied. Likewise, rapid urbanization has resulted in tremendous increase in vector density as a result of human activities that promote mosquito breeding.[11] According to Papa et al.,[12] it is common in serologic testing for cross-reactions to occur among flaviviruses such as Dengue virus (DENV) and tick-borne encephalitis virus; this necessitates caution when evaluating serologic results of flaviviral infections. Therefore, this study was able to determine pure West Nile virus antibodies and occurrence of cross reactivity according to DOHMH,[5] that a positive test for West Nile IgG in the absence of a positive West Nile IgM is indicative of a previous flavivirus infection and is not by itself evidence of an acute
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O. E. Kolawole and O. J. Kola
West Nile virus infection. The present seroprevalence study of West Nile virus antibodies in Ogbomoso environs has been able to provide useful information on the seroepidemiology of the virus in Ogbomoso. The study shows an exposure to the areas of the community where epidemiological and environmental surveillance is needed. There is currently no human West Nile vaccine, specific treatment, or method to block the bird–mosquito transmission cycle. Therefore, although potentially costly, effective surveillance and preventive efforts are needed and are likely to be less than the costs associated with responding to major West Nile virus outbreaks. The result of this study showed the seroprevalence of WNV IgG 18(19.4%) is higher than WNV IgM 12(12.9%). People should be educated on personal protective measures that can be taken to greatly reduce the risk of being bitten by infected mosquitoes and the government should implement a more effective epidemiological and environmental surveillance system. REFERENCES 1. Nash. D.; Mostashari, F.; Fine, A. The Outbreak of West Nile Virus Infection in the New York City Area in 1999. N. Engl. J. Med. 2001, 344(24), 1807–1814. 2. Paz, S. The West Nile Virus Outbreak in Israel (2000) from a New Perspective: The Regional Impact of Climate Change. Int. J. Environ. Health Res. 2006, 16(1), 1–13. 3. Steinman, A.; Banet-Noach, C.; Tal, S.; Levi, O.; Simanov, L.; Perk, S.; Malkinson, M.; Shpigel, N. West Nile Virus Infection in Crocodiles. Emerg. Infect. Dis. 2003, 9(7), 887–889. 4. Tyler, K.L.; Pape, J.; Goody, R.J.; Corkill, M. Kleinschmidt-DeMasters, B.K. CSF Findings in 250 Patients with Serologically Confirmed West Nile Virus Meningitis and Encephalitis. Neurology 2006, 66(3), 361–365. 5. Department of Health and Mental Hygiene. DOHMH (2012) Advisory #8: West Nile Virus, New York. 6. Lindsey, N.P.; Staples, J.E.; Lehman, J.A.; Fischer, M. Medical Risk Factors for Severe West Nile Virus Disease, United States, 2008–2010. Am. J. Trop. Med. Hyg . 2012, 87 (1), 179–184. 7. Pealer, L.N.; Marfin, A.A.; Petersen, L.R.; Lanciotti, R.S.; Page, P.L.; Stramer, S.L.; Stobierski, M.G.; Signs, K.; Newman, B.; Kapoor, H.; Goodman, J.L.; Chamberland, M.E. Transmission of West Nile Virus through Blood Transfusion in the United States in 2002. N. Engl. J. Med. 2003, 349(13), 1236–1245. 8. Nett, R.J.; Kuehnert, M.J.; Ison, M.G.; Orlowski, J.P.; Fischer, M.; Staples, J.E. Current Practices and Evaluation of Screening Solid Organ Donors for West Nile Virus. Transpl. Infect. Dis. 2012, 14(3):268–277. 9. Omilabu, S.A.; Olaleye, O.D.; Aina, Y.; Fagbami, A.H. West Nile Complement Fixing Antibodies in Nigeria Domestic Animals and Humans. J. Hyg. Epidemiol. Microbiol. Immunol. 1990, 34(4), 357–363 10. Healy, J.; Reisen, W.K.; Kramer, V.; Barker, C.M. Do Current Surveillance Methods Provide Adequate Warning for Human Infections with West Nile Virus? Proc. Mosq. Control Assoc Calif . 2012, 80, 17–21 11. Monath, T.P.; Dengue: The Risk to Developed and Developing Countries. Proc. Nat. Acad. Sci. USA. 1994, 91, 2395–2400. 12. Papa, A.; Karabaxoglou, D.; Kansouzidou, A. Acute West Nile Virus Neuroinvasive Infections: Cross-Reactivity with Dengue Virus and Tick-Borne Encephalitis Virus. J. Med. Virol. 2011, 83(10), 1861–1865. doi:10.1002/jmv.22180.
