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Ultra-violet radiation is responsible for the differences in global epidemiology of chickenpox and the evolution of varicella-zoster virus as man migrated out of Africa.

Rice PS - Virol. J. (2011)

Bottom Line: Primary infection is much less common in children in the tropics compared with temperate areas.This results in increased adult susceptibility causing outbreaks, for example in health-care workers migrating from tropical to temperate countries.This is supported by the observation that temperate genotypes are found in the tropics only in specific circumstances, namely where ultra-violet radiation has either been excluded or significantly reduced in intensity.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Medical Microbiology, St George's Hospital, Blackshaw Road, London, SW17 0QT, UK. price@sgul.ac.uk.

ABSTRACT

Background: Of the eight human herpes viruses, varicella-zoster virus, which causes chickenpox and zoster, has a unique epidemiology. Primary infection is much less common in children in the tropics compared with temperate areas. This results in increased adult susceptibility causing outbreaks, for example in health-care workers migrating from tropical to temperate countries. The recent demonstration that there are different genotypes of varicella-zoster virus and their geographic segregation into tropical and temperate areas suggests a distinct, yet previously unconsidered climatic factor may be responsible for both the clinical and molecular epidemiological features of this virus infection.

Presentation of the hypothesis: Unlike other human herpes viruses, varicella-zoster virus does not require intimate contact for infection to occur indicating that transmission may be interrupted by a geographically restricted climatic factor. The factor with the largest difference between tropical and temperate zones is ultra-violet radiation. This could reduce the infectiousness of chickenpox cases by inactivating virus in vesicles, before or after rupture. This would explain decreased transmissibility in the tropics and why the peak chickenpox incidence in temperate zones occurs during winter and spring, when ultra-violet radiation is at its lowest. The evolution of geographically restricted genotypes is also explained by ultra-violet radiation driving natural selection of different virus genotypes with varying degrees of resistance to inactivation, tropical genotypes being the most resistant. Consequently, temperate viruses should be more sensitive to its effects. This is supported by the observation that temperate genotypes are found in the tropics only in specific circumstances, namely where ultra-violet radiation has either been excluded or significantly reduced in intensity.

Testing the hypothesis: The hypothesis is testable by exposing different virus genotypes to ultra-violet radiation and quantifying virus survival by plaque forming units or quantitative mRNA RT-PCR.

Implications of the hypothesis: The ancestral varicella-zoster virus, most probably a tropical genotype, co-migrated with man as he left Africa approximately 200,000 years ago. For this virus to have lost the selective advantage of resistance to ultra-violet radiation, the hypothesis would predict that the temperate, ultra-violet sensitive virus should have acquired another selective advantage as an evolutionary trade-off. One obvious advantage could be an increased reactivation rate as zoster to set up more rounds of chickenpox transmission. If this were so, the mechanism responsible for resistance to ultra-violet radiation might also be involved in reactivation and latency. This could then provide the first insight into a genetic correlate of the survival strategy of this virus.

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Mean annual sunshine fraction (1961-1990), % of time with bright sunshine and age stratified VZV IgG sero-prevalence.
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Figure 5: Mean annual sunshine fraction (1961-1990), % of time with bright sunshine and age stratified VZV IgG sero-prevalence.

Mentions: A search for sero-epidemiological studies of varicella-zoster virus (VZV) using the terms "varicella", "chickenpox" and "seroepidemiology" produced a total of 25 papers. From these publications other relevant references were also located giving a total of 42 articles, reviewed in [14]. Whilst the studies were of different formats, linear regression curves of age-stratified antibody prevalence plotted against latitude showed a reasonably good fit (r2 ≈ 0.5) was demonstrated across all age groups of children >5 years (Figure 1). The same antibody prevalence data when plotted against temperature, rainfall, population density and sunshine, using data drawn from the World Meteorological Organisation (http://www.wmo.int) and the United Nations (http://www.fao.org/WAICENT/FAOINFO/SUSTDEV/EIdirect/CLIMATE/EIsp0002.htm), showed no consistent correlation (Figures 2, 3, 4 and 5).


Ultra-violet radiation is responsible for the differences in global epidemiology of chickenpox and the evolution of varicella-zoster virus as man migrated out of Africa.

Rice PS - Virol. J. (2011)

Mean annual sunshine fraction (1961-1990), % of time with bright sunshine and age stratified VZV IgG sero-prevalence.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3094303&req=5

Figure 5: Mean annual sunshine fraction (1961-1990), % of time with bright sunshine and age stratified VZV IgG sero-prevalence.
Mentions: A search for sero-epidemiological studies of varicella-zoster virus (VZV) using the terms "varicella", "chickenpox" and "seroepidemiology" produced a total of 25 papers. From these publications other relevant references were also located giving a total of 42 articles, reviewed in [14]. Whilst the studies were of different formats, linear regression curves of age-stratified antibody prevalence plotted against latitude showed a reasonably good fit (r2 ≈ 0.5) was demonstrated across all age groups of children >5 years (Figure 1). The same antibody prevalence data when plotted against temperature, rainfall, population density and sunshine, using data drawn from the World Meteorological Organisation (http://www.wmo.int) and the United Nations (http://www.fao.org/WAICENT/FAOINFO/SUSTDEV/EIdirect/CLIMATE/EIsp0002.htm), showed no consistent correlation (Figures 2, 3, 4 and 5).

Bottom Line: Primary infection is much less common in children in the tropics compared with temperate areas.This results in increased adult susceptibility causing outbreaks, for example in health-care workers migrating from tropical to temperate countries.This is supported by the observation that temperate genotypes are found in the tropics only in specific circumstances, namely where ultra-violet radiation has either been excluded or significantly reduced in intensity.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Medical Microbiology, St George's Hospital, Blackshaw Road, London, SW17 0QT, UK. price@sgul.ac.uk.

ABSTRACT

Background: Of the eight human herpes viruses, varicella-zoster virus, which causes chickenpox and zoster, has a unique epidemiology. Primary infection is much less common in children in the tropics compared with temperate areas. This results in increased adult susceptibility causing outbreaks, for example in health-care workers migrating from tropical to temperate countries. The recent demonstration that there are different genotypes of varicella-zoster virus and their geographic segregation into tropical and temperate areas suggests a distinct, yet previously unconsidered climatic factor may be responsible for both the clinical and molecular epidemiological features of this virus infection.

Presentation of the hypothesis: Unlike other human herpes viruses, varicella-zoster virus does not require intimate contact for infection to occur indicating that transmission may be interrupted by a geographically restricted climatic factor. The factor with the largest difference between tropical and temperate zones is ultra-violet radiation. This could reduce the infectiousness of chickenpox cases by inactivating virus in vesicles, before or after rupture. This would explain decreased transmissibility in the tropics and why the peak chickenpox incidence in temperate zones occurs during winter and spring, when ultra-violet radiation is at its lowest. The evolution of geographically restricted genotypes is also explained by ultra-violet radiation driving natural selection of different virus genotypes with varying degrees of resistance to inactivation, tropical genotypes being the most resistant. Consequently, temperate viruses should be more sensitive to its effects. This is supported by the observation that temperate genotypes are found in the tropics only in specific circumstances, namely where ultra-violet radiation has either been excluded or significantly reduced in intensity.

Testing the hypothesis: The hypothesis is testable by exposing different virus genotypes to ultra-violet radiation and quantifying virus survival by plaque forming units or quantitative mRNA RT-PCR.

Implications of the hypothesis: The ancestral varicella-zoster virus, most probably a tropical genotype, co-migrated with man as he left Africa approximately 200,000 years ago. For this virus to have lost the selective advantage of resistance to ultra-violet radiation, the hypothesis would predict that the temperate, ultra-violet sensitive virus should have acquired another selective advantage as an evolutionary trade-off. One obvious advantage could be an increased reactivation rate as zoster to set up more rounds of chickenpox transmission. If this were so, the mechanism responsible for resistance to ultra-violet radiation might also be involved in reactivation and latency. This could then provide the first insight into a genetic correlate of the survival strategy of this virus.

Show MeSH
Related in: MedlinePlus