If you look at the evidence to date from a different perspective, a virologist at St George’s Hospital, University of London in the UK believes it suggests the sun’s UV rays inactivate the chickenpox virus on the skin before it has a chance to transmit to another person, thus explaining why the disease spreads less readily in tropical countries. Dr Phil Rice told the press last week he hopes his findings will lead to new ways to prevent chickenpox and its more severe cousin, shingles.

The idea that ultraviolet (UV) rays can inactivate viruses is not new, but this is the first time that such firm conclusions have been made in connection with the varicella-zoster virus, the herpes virus responsible for chickenpox and shingles.

Writing about his work earlier this year in Virology Journal, Rice shows how chickenpox is much less common in parts of the world with high levels of UV rays compared with places where the levels are low, and why in temperate zones, the disease peaks in winter and spring, when UV rays are at their lowest.

The findings challenge a widely held view that geographical differences in the spread of chickenpox are due to other factors such as population density, heat, humidity and being infected with other viruses that guard against varicella-zoster.

For his investigation, Rice looked at evidence from 25 studies on the prevalence of varicella-zoster virus. These had examined disease patterns in both temperate and tropical regions around the world.

He examined the patterns relative to a range of climatic variables to find the one that most strongly correlated with them. After ruling out other factors, he found UV rays was the only variable most strongly linked to the infection patterns in each of the countries studied.

Rice 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.”

He said what helped to convince him was that whenever there was an anomaly in the data, there was a plausible explanation. For instance, in India and Sri Lanka, chickenpox peaks in the hot, dry, sunny season. Now, at first, you might expect this also to be when the UV rays were strongest, thus disproving the link, but, that is not the case:

“… UV rays are actually much lower in the dry season compared with the monsoon period. In the dry season, the pollution in the atmosphere reflects the UV rays back into space before they reach us. But in monsoon season, the rains wash away the pollution, meaning the UV rays can get through,” he explained.

Rice’s findings also appear to show why two quite different genotypes of varicella-zoster virus have evolved: one for temperate climes and one for the tropics.

He found the genotype that is prevalent in the temperate regions of the globe only spreads when the UV radiation is either reduced, or shielded in some way. For example, it would spread indoors, but not out of doors.

But the genotype that spreads in the tropics seems to be able to do this despite the presence of some UV light. Rice believes the tropical genotype has retained resistance to UV radiation, and that this resistance has been lost in the temperate one, which broke off from the tropical one some time ago.

But viruses don’t survive by losing an advantage unless they have “sacrificed” it for a higher gain. Rice reckons the temperate virus traded in UV resistance for the greater advantage of being able to reactivate more easily, which is what happens with shingles.

“The virus can only have one of these survival advantages, not both. This might explain why shingles appears to be so much less common in people from the tropics, and why the temperate virus reactivates much more readily than the tropical type,” he suggests.

The current chickenpox vaccine was developed in the 1970s, before we knew there were two genotypes of varicella-zoster virus.

Rice believes these findings will help find new treatments for chickenpox and shingles, and that more research should now be done to determine the underlying mechanism by which UV radiation affects the virus.

Anyone who has had chickenpox can get shingles, a painful complaint that develops as a rash along a band of skin supplied by the nerve that the virus infects. It is thought that about one in five people who has had chickenpox will develop shingles at some time in their lives, sometimes after a period of illness or stress can trigger it, although more commonly after the age of 50, when the immune system, which normally keeps the virus in check, slows down.

Written by Catharine Paddock PhD