Ascoviruses (proposed family Ascoviridae: Federici, 1983) are as yet unclassified (Miller, 1998) but probably do represent a distinct family. They are dsDNA viruses that possess a large genome and a unique hexagonally patterned envelope. Although not occluded in a single-protein matrix, the ascovirus virions are intermixed with proteins and microvesicles to form a vesiculate occlusion body (Tanada and Kaya, 1993). The ascoviruses cause hypertrophy of host nuclei and cells in their lepidopteran hosts (Federici, 1983) and, eventually, the nucleus ruptures. Cytoplasmic membranes form in sheets in the cell and result in the formation of vesicles that are released into the host tissues and hemolymph when the cell basement membranes break down. Ascoviruses infect a range of tissues but the fat body is always infected. Infections are typically chronic, producing color changes in the host and difficulties in molting. Mortality occurs in 12-21 days post infection. These viruses appear to be more efficiently transmitted via parasitoids than orally (Tanada and Kaya, 1993) and have only been isolated from Lepidoptera and one ichneumonid wasp (Bigot et al., 1997).

Iridoviruses (Family Iridoviridae) are large, nonenveloped, nonoccluded dsDNA viruses that are icosahedral in shape. The name is derived from "iridescent virus", which refers to the characteristic microcrystalline lattice arrangement of virions in the host cells that result in Bragg reflection of visible light (Williams and Smith, 1957). Iridoviruses are found in both vertebrate and invertebrate animals and currently are assigned to the same genus (Iridovirus) except for one isolate from a mosquito (Chloriridovirus) (Williams, 1998). This family of viruses has been isolated from Coleoptera, Diptera, Hemiptera, Lepidoptera (Hall, 1985), and Orthoptera (Boucias et al., 1987), as well as some noninsect arthropods. Most iridoviruses are not transmitted transovarially and are not easily transmitted orally. Transmission may depend on massive dosages that might be encountered due to cannibalism or on mechanical transmission by parasitoids (Williams, 1998). Infections tend to be systemic but the fat body and epidermis of hosts are particularly affected. Although chronic in nature, virus infection is usually lethal. The nuclei of cells are destroyed resulting in the destruction of hemocytes.

One genus in the family Parvoviridae has been recovered from insects, Densovirus (DNV). First isolated from the waxworm, Galleria mellonella, these viruses have now been recovered from Diptera, Orthoptera, Blattodea, Odonata, and other Lepidoptera (Kawase, 1985). This ssDNA, nonenveloped virus is characterized by its effects on the nucleus of host cells, and it attacks most host tissues. Infection results in extreme hypertrophy of cell nuclei and the filling of the nuclei with small isometric particles. The nuclei become strongly eosinophilic (dense nuclei, thus the name densovirus). Discoloration and paralysis of the host often occur. These viruses can be very virulent and infectious, and the type species, GmDNV, has caused serious problems for the waxworm bait industry in the Midwest in recent years. Despite their high virulence, densoviruses do not replicate in vertebrates (Bergoin and Tijssen, 1998).

The polydnaviruses are enveloped, double-stranded, polydisperse DNA viruses (thus the name poly-DNA-virus), which are unique due to the obligately mutualistic relationship with their hymenopteran hosts. Although new studies suggest that viruses found in other parasitic Hymenoptera may belong in the polydnavirus group, polydnaviruses are recognized only in several genera of ichneumonid and braconid hosts (Webb, 1998). Polydnaviruses are divided into two genera, Bracovirus from braconid hosts, and Ichnovirus from ichneumonid hosts (Tanada and Kaya, 1993). The genera are related but are divergent genetic lines. Relationships of the viruses within host genera parallel those of their hosts, expected because the virus is integrated into the wasp host DNA as proviral DNA and is inherited by progeny (Whitfield, 1997). Polydnaviruses excise from the host genome and replicate only in the calyx of the host ovaries. There are no known pathogenic effects on the wasp host. When the female wasp oviposits into the host, the virus particles are secreted with the eggs. The virus enters the host tissue cells, primarily the hemocytes, fat body, muscle and tracheal cells (Stoltz and Vinson, 1979). It does not replicate in these tissues but acts to suppress the host immune system, possibly in conjunction with teratocytes and wasp venoms. Immune suppression and host developmental delays that result favor the survival of the parasite eggs and larvae (Tanada and Kaya, 1993) and, in fact, may be required for survival of the parasitoids (Webb, 1998).

Poxviridae, enveloped dsDNA viruses, are found in vertebrates as well as invertebrates and the two groups have morphological and genetic similarities (King et al., 1998). The insect-specific poxviruses, the entomopoxviruses (EPV), however, are occluded much like the baculoviruses into protein matrices called spheroids . The occlusion bodies arose independently in the poxviruses as well as in the baculoviruses and the reoviruses, probably as protection from environmental degradation. EPVs have been found infecting Coleoptera (Genus A), Lepidoptera and Orthoptera (Genus B), Diptera (Genus C), and Hymenoptera (unclassified) (Arif, 1984; King et al., 1998). Lepidoptera infected with EPV show swelling and whitening due to infection of fat body cells, which causes cell proliferation and hypertrophy. Mortality is not rapid, larvae may live from 12-72 days after infection occurs, and development of infection may be even slower in Coleoptera (Tanada and Kaya, 1993).