Infection of its lepidopteran host by the Helicoverpa armigera stunt virus (Tetraviridae)

Abstract

Techniques of microscopy and histopathology were employed to study the positive-sense, single-stranded RNA virus, the Helicoverpa armigera stunt virus (HaSV; omegatetravirus, Tetraviridae) infecting its caterpillar host. Infection of the virus per os during the first three instars of larval development is virulent and leads to rapid stunting and mortality. In contrast, no detectable symptoms occur in later larval development, signifying a high degree of developmental resistance. A quantitative study of cell populations in the host midgut during this time showed that increased cell numbers during development alone could not account for the increase in resistance. HaSV infection was restricted to the midgut and three of its four cell types. In younger larvae, the virus initiated its infection in closely situated foci that appeared to expand to link with others to cover larger areas of the midgut. The midgut cells of the infected larvae responded with an increased rate of sloughing to an extent rendering the midgut incapable of maintenance or recovery of normal function. In contrast, infection of older larvae by HaSV did not lead to overt pathology although foci of HaSV infection were detected in their midguts. However, the foci were more sparsely situated, failed to expand, and eventually disappeared, presumably due to cell sloughing. These observations indicate that cell sloughing is an immune response existing throughout larval development but midguts of older larvae have an additional mechanism to account for the increased resistance. This second mechanism results in midgut cells becoming more refractory to infection and, combined with cell sloughing, allows the midguts of older larvae to recover more readily from HaSV infection. These two mechanisms are similar to those seen with host responses to baculoviruses, which display developmental resistance to a lesser degree against more general infections. HaSV remaining in the midgut appears to amplify the degree of developmental resistance.