Influence of Oxygen Tensions in Viral Infections

Excerpt from Chapter 16: Effects of Hyperbaric Oxygen in Infectious Diseases: Basic Mechanisms in Hyperbaric Medicine Practice 4th edition, Harry T. Whelan and Eric P. Kindwall, editors

With flu season among us, you may find the following information helpful from Hyperbaric Medicine Practice 4th Edition.

Presently there is no evidence of direct beneficial effects of HBO2 in viral infections. However, it appears that oxygen tensions affect the growth and virulence of certain viruses. Hypoxia (3% O2) causes marked alterations in growth characteristics of some viruses. Plaque diameter and plating efficiency of adenoviruses cultured under hypoxic conditions are markedly reduced. In contrast, polioviruses are not adversely affected by hypoxic conditions. Replication of rubella virus in hamster kidney cells was not altered during exposure to oxygen tensions ranging from 1 to 330 mmHg.

Reactive oxygen species cause single-strand breaks in DNA. Viral DNA may be particularly susceptible to oxidative damage because viruses lack antioxidants and DNA repair mechanisms. Exogenous SOD and catalase combine to confer protection against inactivation of viruses. Therefore, it is possible that antioxidants in the host cells may protect viruses against free radicals. Thus, exogenous antioxidants may account, at least in part, for the viral resistance to hyperoxia.

Effects of various oxygen tensions in murine models of viral infections have been examined. In a model of encephalomyocarditis caused by the MM virus, hypobaric hypoxia (21% O2 at 0.5 ATA) significantly increased mortality as compared to normoxia. Exposure to hypobaric normoxia (100% O2 at 0.2 ATA) also increased mortality in mice infected with influenza A virus. However, neither normobaric hypoxia (11% O2 at 1 ATA) nor hyperoxia (77% O2 at 1 ATA) altered mortality. Thus, it appears that decreased atmospheric pressure, rather than oxygen tension, influenced mortality due to influenza A virus in that study. In contrast, Ayers et al. found that exposure to hyperoxia (99% O2 at 1 ATA) resulted in influenza-infected mice dying 3 to 4 days earlier than normoxic controls. One possible explanation is the finding by Naldini et al. that the antiviral activity of interferon-alpha (and interferon-gamma) is decreased in vitro under “normoxic” conditions (140 mmHg O2) compared to “hypoxic” conditions (14 mmHg O2). Exposure to hypoxia (11% O2) increased mortality and viral titers in tissue of mice infected with Coxsackie B-1 virus. Interestingly, hypobaric hypoxia (21% O2 at 0.5 ATA) increased viral titers, but not mortality. In addition, HBO2 (100% O2 at 3 ATA) enhanced mortality in mice infected with Coxsackie B-1 virus. Pretreatment of mice with HBO2 significantly increased viral titers in heart muscle and brown fat by three days after inoculation of the virus. The effects of HBO2 may have been mediated through free radicals since, in another model of Coxsackie B3 myocarditis, polyethylene-conjugated SOD reduced cellular infiltration, myocardial necrosis, and calcification scores, compared to the control group at day 14, after intraperitoneal challenge in C3H/He mice. There were no differences in viral titers among the three groups at day 7 and viral titers were no longer detected by day 14 in any of the treatment groups.

Another recent study investigated the basis of treating chronic hepatitis with HBO2 and to compare the changes in hepatic function, immunity, pathologic morphology, ultrastructure and HBV in hepatic tissues before and after treatment. The experimental group was treated with six courses of HBO2 while the control group was treated for 60 days with standard therapy. There were significant differences between the experimental and control groups after treatment; for the experimental group, all markers of hepatic function and hepatocyte degeneration or necrosis were decreased, but the fibrosis and fat-storing cells in the liver were not reduced.

In summary, oxygen tensions appear to influence the outcome of viral infections in animal models. Hyperoxia appears to increase mortality in mice infected with influenza A virus or Cocksackie B-1 virus. Hypoxic conditions also increase mortality in Coxsackie B-1 infected mice. Treatment of chronic HBV with HBO2 appears to be effective, and should be considered as an adjunct to standard pharmacologic therapy. HBO2 has not been shown to be effective at reversing liver fibrosis.

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