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The West Nile virus epidemic of 2012, the worst in a decade, may be notorious for yet another reason: The virus, in some cases, is attacking the brain more aggressively than in the past, raising the specter that it may have mutated into a nastier form, say two neurologists who have extensive experience dealing with the illness “I’ve been struck this year that I’m seeing more patients where the brain dysfunction has been very much worse,” said Angus, of Detroit’s Henry Ford Hospital.
“It makes you wonder if something’s different, if something’s changed.” And while the virus in the past has typically invaded the brain and spinal cord only of people who have weakened immune systems, such as the elderly and transplant or cancer patients, Angus this summer treated a severely affected woman in her 20s and a man in his 40s. Leis said he is seeing much more severe encephalitis — inflammation of the brain — than he has in the past. “It is clearly much more neuroinvasive, neurovirulent,” he said. Four patients Leis treated this summer had lost their ability to talk or write. Another was paralyzed on one side, as often seen in strokes, not West Nile infections. Others experienced recurring seizures.
Last month, Leis asked a Food and Drug Administration scientist who studies the genetics of the virus whether a new, more virulent strain was circulating.
“You are absolutely right . . . that new genetic variants of WNV might have appeared this year,” the scientist replied in an Oct. 23 e-mail obtained by The Washington Post. The scientist continued that “it is not easy to correlate” the new mutations with any specific type of brain damage.
Thirty minutes after Leis received the message, another e-mail from the same scientist arrived. It said the previous message had been “recalled.” When contacted by phone, the FDA scientist, who works at the agency’s Center for Biologics Evaluation and Research, declined to discuss the messages, saying that his superiors had instructed him not to talk to reporters.
West Nile virus: the complex biology of an emerging pathogen.
West Nile virus (WNV) is a zoonotic virus that circulates in birds and is transmitted by mosquitoes. Incidentally, humans, horses and other mammals can also be infected. Disease symptoms caused by WNV range from fever to neurological complications, such as encephalitis or meningitis. Mortality is observed mostly in older and immunocompromised individuals. In recent years, epidemics caused by WNV in humans and horses have become more frequent in several Southern European countries, such as Italy and Greece. In 1999, WNV was introduced into the USA and spread over North America within a couple of years. The increasing number of WNV outbreaks is associated with the emergence of novel viral strains, which display higher virulence and greater epidemic potential for humans. Upon infection with WNV, the mammalian immune system counteracts the virus at several different levels. On the other side, WNV has developed elaborated escape mechanisms to avoid its elimination. This review summarizes recent findings in WNV research that help to understand the complex biology associated with this emerging pathogen.
The Molecular Evolution of Lineage 2 West Nile Virus.
Since the 1990's West Nile virus (WNV) has become an increasingly important public health problem and cause of outbreaks of neurological disease. Genetic analyses have identified multiple lineages with many studies focusing on lineage 1 due to its emergence in New York in 1999 and neuroinvasive phenotype. Until recently, viruses in lineage 2 were not thought to be of public health importance due to few outbreaks of disease being associated with viruses in this lineage. However, recent epidemics of lineage 2 in Europe (Greece, Italy) and Russia have shown the increasing importance of this lineage. There are very few genetic studies examining isolates belonging to lineage 2. We have sequenced the full-length genomes of four older lineage 2 WNV isolates, compared them to 12 previously published genomic sequences, and examined the evolution of this lineage. Our studies show that this lineage has evolved over the last 300-400 years and appears to correlate with a change from mouse attenuated to virulent phenotype based on previous studies by our group (Beasley et al. 2004. Molecular determinants of virulence of West Nile virus in North America. Arch Virol Suppl, 35-41). This evolution mirrors that which is seen in lineage 1 isolates, which have also evolved to a virulent phenotype over the same period of time.