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Tips from the Journals of the American Society for Microbiology: March 2001

MONKEYS DON'T DEVELOP AIDS DESPITE HIGH VIRUS LEVELS

African green monkeys do not develop AIDS despite high levels of the simian immunodeficiency virus (SIV) in their blood, a surprising finding that challenges some commonly held beliefs about how the virus and its cousin, HIV, cause disease. Researchers from the Southwest Foundation for Biomedical Research and Emory University report their results in the March 2001 issue of the Journal of Virology.

SIV and HIV have long been thought to cause disease by replicating at a high rate inside immune cells, eventually overtaxing the immune system and causing it to fail. This model of AIDS is supported by evidence that progression to AIDS in humans is measured by a decline in CD4 immune cells which is associated with high levels of the virus in the blood. Antiviral drug treatment, which reduces the level of virus in the blood, stops and most often reverses progression of the disease.

Scientists have known for years that African green monkeys can be infected with SIV and not develop AIDS but it was believed that this was due to effective immune system control of the virus, which would appear as a low viral load in the blood. The researchers in this study, though, found high levels of the virus in the blood of all the infected monkeys. They also found high levels of viral replication in the central nervous system, believed to be the primary cause of neurological wasting, without any symptoms in the monkeys.

"These data clearly indicate that high levels of viremia and high rates of virus replication do not necessarily lead to disease and that specific host factors or the particular nature of the host response plays a critical role in determining whether disease arises following infection," say the researchers.

(S. Broussard, S. Staprans, R. White, E. Whitehead, M. Feinberg and J. Allan. 2001. Simian immunodeficiency virus replicates to high levels in naturally infected African green monkeys without inducing immunologic or neurologic disease. Journal of Virology, 75: 2262-2275.)

CRYPTOSPORIDIUM FOUND IN WOODLAND CREATURES

Watch out. Those innocent woodland creatures could be harboring the Cryptosporidium parasite, say researchers from Columbia University. They report their findings in the March 2001 issue of the journal Applied and Environmental Microbiology.

"We performed a wildlife survey, focusing on white-tailed deer and small mammals, to assess whether they may serve as environmental sources of Cryptosporidium," say the researchers. They collected fecal samples from several locations in lower New York State over a two year period and tested them for the parasite. They found evidence of the parasite in samples from white-tailed deer, chipmunks, skunks, racoons and muskrats.

"These data provide evidence that there is sylvatic transmission of Cryptosporidium parvum involving deer and other small mammals. This study affirmed the importance of wildlife as potential sources of Cryptosporidium in the catchments of public water supplies," say the researchers.

(J. Perz and S. Le Blancq. 2001. Cryptosporidium parvum infection involving novel genotypes in wildlife from lower New York State. Applied and Environmental Microbiology, 67: 1154-1162.)

SWINE COULD BE RESERVOIR FOR HEPATITIS

Pigs experimentally infected with a human strain of the hepatitis E virus (HEV) develop the disease, suggesting that swine could serve as an environmental reservoir for the disease, say researchers from Iowa State University, Virginia Polytechnic Institute and the National Institutes of Health in the March 2001 issue of the Journal of Clinical Microbiology.

HEV is the leading cause of non-A, non-B hepatitis in developing countries and is not believed to be endemic in the United States, but sporadic cases have been reported and anti-HEV antibodies have been found in a significant proportion of healthy people. Several years ago, scientists discovered a strain of HEV in pigs that was genetically similar to human HEV, suggesting that pigs could be reservoirs for human strains as well.

To test this theory, the researchers experimentally infected groups of pigs with either the human or the swine strain of HEV. After nearly two months the pigs that were infected with the human strain had more severe liver damage than those infected with the swine strain, and they were shedding infectious virus in their feces.

"Since HEV was shed in the feces of infected pigs, exposure to feces from infected pigs represents a risk for transmission of HEV, and pigs should be considered a reservoir for HEV," say the researchers.

(P. Halbur, C. Kasorndorkbua, C. Gilbert, D. Guenette, M. Potters, R. Purcell, S. Emerson, T. toth and X.J. Meng. 2001. Comparative pathogenesis of infection of pigs with hepatitis E viruses recovered from a pig and a human. Journal of Clinical Microbiology, 39: 918-923.)

Copies of the above articles can be accessed online through http://www.asmusa.org/pcsrc/tip.htm.

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