Helicoverpa zea nudivirus 2 (HzNV-2, Hz-2V, gonad specific virus [GSV], or Heliothis zea nudivirus 2) is an enveloped, rod-shaped, nonoccluded, double stranded DNA (dsDNA) sexually transmitted virus whose natural host is the corn earworm moth. At about 440 by 90 nm, it is the causative agent of a sexually transmitted viral disease for the species. It was originally identified in a colony of corn earworm moths established and maintained in Stoneville, Mississippi, U.S. and was found to be responsible for the sterility of those infected. The virus does not always cause sterility, though. Many moths are asymptomatic carriers of the virus. Infected female hosts mate much more than those uninfected. With more mating events, the virus spreads to several males. Fertile female hosts may also pass the virus on through their eggs. HzNV-2 is closely related to HzNV-1; it is likely that HzNV-1 is a variant of HzNV-2 which exists in a persistent state in infected moths. HzNV-2 was discovered in 1995. Originally, symptomatic hosts were described as being "agonadal". Then, the virus was given the name "gonad specific virus". It was later given the name "Helicoverpa zea nudivirus 2" because of the similar physical properties between it and HzNV-1, which had been described about 20 years prior. It is highly unlikely that the common effects of HzNV-2 on their hosts, malformed reproductive tissues causing infertility, would have been selected for establishing an ovarian cell line. It is more likely that those chosen moths were asymptomatic. Their common ancestor is believed to share a common ancestor with baculoviruses, a family of viruses whose natural hosts are decapods, arthropods, Hymenoptera, Diptera, and Lepidoptera.
Pathology The natural host of HzNV-2 is the corn earworm moth (Helicoverpa zea). The virus is spread to offspring through their mothers' eggs (Vertical transmission) and through mating attempts between adult moths (Horizontal transmission). Infected moths are referred to as either asymptomatic (AS) or agonadal (AG), due to the virus causing larvae to never form functional gonads. HzNV-2 is very common among wild moths, and it is very able to survive in host populations.
Asymptomatic carriers Persistent replication of HzNV-2 in insect hosts make asymptomatic (AS), fertile carriers. Unlike baculoviruses, the productive replication of this virus does not kill the hosts. Instead, it causes malformed gonads, sterilizing the hosts. When healthy females mate with infected males, the offspring are infected through the eggs (transovarially). Typically, some of the offspring are infertile while others are infected, AS carriers. Whether or not the offspring is AS or agonadal is dependent on how much viral particle content they receive from their mothers. The amount of virus mothers spread to their children increases over the time of infection. In fact, most infected, wild female moths are fertile and AS carriers, and infected females account for up to 69% of all wild females. When they mate with sterile, infected moths are still able to spread the virus through mating. After mating, the virus productively replicates inside the females, which makes the viral dose increase on successive oviposition days. These abilities to spread differently through hosts that are both asymptomatic and symptomatic and that spread the virus vertically to offspring and horizontally to mates makes HzNV-2 very fit and able to coexist well in the wild with its host.
Symptomatic hosts HzNV-2 is able to change the molecular processes of their hosts. Though infected larvae appear to be very normal, when they emerge from their cocoons as adults, they may be without gonads. This condition is described as being "agonadal". The reproductive systems of both sexes are malformed and appear as a large "Y" shape. Female hosts infected through vertical transmission often do not develop several reproductive structures, including their ovaries, bursa copulatrix, accessory glands, and spermatheca. In addition, their common and lateral oviducts are malformed and enlarged. Viral replication in female gonads result in hypertrophy of the oviducts and proliferation of the cells making up these tissues. These enlargements appear to begin as early as their last instar as larvae. The lateral oviducts of healthy, adult female moths areone or two cell layers; those of infected female moths have four to eight layers instead. These enlargements may increase virus production. HzNV-2 also causes the formation of a "viral plug" that prolongs their mating behaviors and serves as a source of contamination for males attempting to mate. Infected females also produce five to seven times more sex pheromone than those uninfected and attract two times as many mates. While mating, female moths will continue to call to other males, uncharacteristic of the species. Since the virus can spread horizontally through sex, this transmits it quicker. Infected males may grow to have small, unfused testes, no seminal vesicles, vas deferencia, or accessory glands. Accessory glands produce pheromonostatic peptide (PSP), which inhibits the amount of mating pheromones females make. Without PSP, female moths continue to attract more partners. The tissues needed for the initiation of copulation and the transfer of reproductive fluids during mating function normally. The lumen of the primary simplex of infected male moths is greatly filled with virus particles that they very likely transmit to healthy females without fertilizing them.
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