The Lancet Neurology, Volume 11, Issue 1, Pages 14 – 15, January 2012
Eugene O Major, Avindra Nath
Each year, the highest incidence of microbial infections in the nervous system is caused by pathogens such as meningococcus, toxoplasmosis, and Cryptococcus, and by encephalitic viruses such as those that cause Japanese encephalitis. For example, this year an outbreak of viral encephalitis in northern India resulted in 2300 hospital admissions and over 400 deaths.1 The herpes virus family also accounts for many cases of encephalitic infections, as does influenza virus, with the likelihood of encephalitic infections relating each year to the severity of the pandemic. However, notable in 2011 was the occurrence of infections that might be considered unanticipated and that were linked either to globalisation, which readily spreads infectious agents between countries, or to new treatments that alter immune physiology.
In a recent study, the investigator2 described the emerging pattern of the breakdown of geographical barriers and the introduction of species into new environments. West Nile virus was used as an example of such infectious intrusions, spreading into North America from Africa as a vector-borne infection. Over a 10 year period, nearly 2 million people were infected, which resulted in over 10 000 cases of encephalitis and meningitis. Remarkably, it took only 4 years for the West Nile virus to cross continental USA from the East to the West coast. Other such vector-borne agents that can be neurotropic, including dengue, yellow fever, and Chikungunya, have also been predicted to spread in future. These are all RNA-containing viruses that seem to travel readily in mosquitoes or infected hosts. In 2011, HIV-1, another well travelled global neurotropic RNA virus, remains a substantial cause of encephalopathy-associated symptoms, which are estimated to occur in at least 50% of HIV-1 infected individuals.3
Pandemic effects in Contagion
Also of increasing concern are serious adverse events associated with biological therapies, notably monoclonal antibodies that modulate the immune system. The human polyomavirus JC virus induces demyelinating diseases, including progressive multifocal leukoencephalopathy (PML).4 PML is directly linked with the use of natalizumab, a humanised IgG4 monoclonal antibody, which is an α4 integrin inhibitor that prevents extravasation of inflammatory cells into the brain and the gut. Natalizumab is an effective treatment for relapsing—remitting multiple sclerosis. However, the incidence of PML in patients with a history of immune suppressive drug treatment and exposure to JC virus is about one in 200, which is close to that reported in patients with AIDS.5
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