No abstract

Cytotoxic T cells are present in the lungs and the bronchoalveolar washings of mice infected intravenously (i.v.) or intranasally (i.n.) with live influenza A/WSN virus. After i.v. injection, cytotoxic T cell activity in both spleens and lungs reaches a peak at 6 days when the level of infectious virus recovered from the lungs falls sharply and the mice do not die. If a lethal dose of virus is given intranasally, very high levels of virus appear rapidly in the lungs, and the development of lung consolidation follows slightly behind the appearance of cytotoxic T cells there. When a non-lethal dose of virus is given intranasally, lower levels of virus are found in the lung and the appearance of cytotoxic T cells is delayed. These results suggest that the cytotoxic T cells play a protective role if the level of virus in the lungs does not reach very high levels. After injection of antithymocyte serum, the subsequent level of cytotoxic T cell activity in the lungs was greatly reduced, suggesting that the T cells recovered in lungs had at an earlier stage been circulating cells. However, splenectomized mice develop high levels of cytotoxic T cell activity, after intranasal infection of mice, indicating that the spleen did not contribute substantially to the T cells recovered in the lungs.

This report examines the requirement for infectious virus in the induction of influenza virus-specific cytotoxic T cells. Infectious influenza virus was found to be highly efficient at generating both primary and secondary cytotoxic T-cell response in vivo. Inactivated influenza virus however, failed to stimulate a detectable cytotoxic T-cell response in vivo even at immunizing doses 10(5)-10(6)-fold higher than the minimum stimulatory dose of infectious virus. Likewise inactivated virus failed to sensitize target cells for T cell-mediated lysis in vitro but could stimulate a specific cytotoxic response from primed cells in vitro. Possible requirements for the induction of virus-specific cytotoxic T-cell responses are discussed in light of these observations and those of other investigators.

Transfer of primary or secondary influenza-immune spleen cells to mice infected intranasally with influenza virus resulted in a significant clearance of virus from the lungs and the protection of the recipients from death. The antiviral activity was associated only with intact, viable cells and was not due to carryover of virus. The effector cell population responsible for the antiviral effect was shown to be T cells. Thus, the removal of adherent, phagocytic and Ig+ cells did not affect the antiviral activity, whereas it was destroyed with antitheta serum and complement. Antiviral activity was specific and was best expressed if the virus used to infect the recipients and to generate immune cells was the same strain. Further work will be necessary to define rigorously the role of different viral antigens in cell-mediated immune response to influenza virus infection.

Factors affecting the mechanical transmission of rotavirus by the legs and wings of the housefly, Musca domestica L., were examined in a laboratory study. Rotavirus was picked up when houseflies walked on thin smears of clarified rotavirus suspensions. The addition of glycerol, which increased viscosity of the virus suspension, and particulate human feces slightly increased the proportion of flies contaminated with virus. However, the addition of glycerol greatly reduced the average number of virus particles picked up per fly, whereas feces greatly increased the number of particles. The proportion of flies with virus-contaminated legs, which transferred virus to > 1 contact surface, was increased by longer contact time with the surface and when the contact surface was agar instead of glass. Most virus particles were deposited on 1st contact with the surface. Most flies dislodged virus particles inoculated on the underside of their wings soon after the start of simulated flight. Our data indicated that the nature of the virus-suspending medium has a greater effect on the level of virus contamination than on the ability to become contaminated. The importance of walking as a mode of virus transport depends on the nature of the contact surface, the risk of the contaminated fly settling first on a surface likely to come into contact with humans, and fly numbers.