Effect of nutritional status and of a carcinogenic pox virus infection on interferon producing capacity and mortality

It appears that both certain viruses and neoplasms have several defense mechanisms to protect them against host defense factors. The ability to counteract interferon (INF) activity and decrease interferon production is probably among the most important. We have studied interferon resistance mechanisms of HIV viruses and adenocarcinomas. We found four pathophysiologic factors: 1) introduction of free INF α/β type I receptors into the circulation in concentrations which inactivate endogenous as well as therapeutic INFs; 2) we have isolated a new protein which inactivates INFs; 3) neoplastic cells appear to produce increased amounts of cAMP phosphodiesterases which interfere with INF synthesis; and 4) neoplastic cells produce increased amounts of prostaglandin E₂ (PgE₂) which also interfere with interferon production. Other investigators have found that ebola and pox viruses induce the release of circulating INF receptors. Several other virus and tumor against host defense mechanisms were also reviewed. It was shown that malnutrition increases the susceptibility to Yaba pox viruses in monkeys. This may explain some of our clinical observations in monkeypox infections in Africa. Malnutrition decreased the interferon-producing capacity of white cells. This may be part of the mechanism of action of the effect of malnutrition on Yaba pox virus induced mortality. Yaba virus infection itself decreased the interferon-producing capacity. The lowest levels of interferon production were seen in animals which were both malnourished and Yaba-virus infected. The lowest production capacity was seen in animals that eventually expired.