19 December 2011 Last updated at 00:04 GMT
Sun 'stops chickenpox spreading'
Exposure to sunlight may help impede the spread of chickenpox, claim researchers.
The University of London team found chickenpox less common in regions with high UV levels, reports the journal Virology.
Sunlight may inactivate viruses on the skin, making it harder to pass on.
However, other experts say that other factors, including temperature, humidity, and even living conditions are equally likely to play a role.
The varicella-zoster virus is highly contagious, while it can be spread through the coughs and sneezes in the early stages of the infection, the main source is contact with the trademark rash of blisters and spots.
UV light has long been known to inactivate viruses, and Dr Phil Rice, from St George's, University of London, who led the research, believes that this holds the key why chickenpox is less common and less easily passed from person to person in tropical countries.
It could also help explain why chickenpox is more common in the colder seasons in temperate countries such as the UK - as people have less exposure to sunlight, he said.
He examined data from 25 earlier studies on varicella-zoster virus in a variety of countries around the world, and plotted these data against a range of climatic factors.
This showed an obvious link between UV levels and chickenpox virus prevalence.
Even initially confusing results could be explained - the peak incidence of chickenpox in India and Sri Lanka is during the hottest, driest and sunniest season.
However, Dr Rice found that, due to atmospheric pollution, UV rays were actually much lower during this season compared with the rainier seasons.
He said: "No-one had considered UV as a factor before, but when I looked at the epidemiological studies they showed a good correlation between global latitude and the presence of the virus."
Professor Judy Breuer from University College London said that while UV could well be contributing to the differences in the prevalence of chickenpox between tropical and temperate regions, there were other factors which needed to be considered.
She said: "Lots of things aside from UV could affect it - heat, humidity and social factors such as overcrowding.
"It's quite possible that UV is having an effect, but we don't have any firm evidence showing the extent this is happening."
Virol J. 2011 Apr 23;8:189.
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.
Department of Medical Microbiology, St George's Hospital, Blackshaw Road, London, SW17 0QT, UK. email@example.com.
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.
PMID: 21513563 [PubMed - indexed for MEDLINE] PMCID: PMC3094303
|<< 前記事(2011/12/23)||ブログのトップへ||後記事(2012/01/04) >>|
|<< 前記事(2011/12/23)||ブログのトップへ||後記事(2012/01/04) >>|