| Hytrosaviridae | |
|---|---|
 | |
| Schematic drawing | |
Virus classification  | |
| (unranked): | Virus |
| Class: | Naldaviricetes |
| Order: | Lefavirales |
| Family: | Hytrosaviridae |
| Genera | |
Hytrosaviridae is a family of double-stranded DNA viruses that infect insects. [1] [2] [3] The name is derived from Hytrosa, sigla from the Greek Hypertrophia for 'hypertrophy' and 'sialoadenitis' for 'salivary gland inflammation.'
The viruses in this family are non occluded, enveloped, rod-shaped virions measuring 500–1,000 nanometers (nm) in length and 50–80 nm in diameter. [4] The virions contain a thin, dense central nucleocapsid that encases the DNA-protein core. The nucleocapsid core is surrounded by an amorphous proteinaceous tegument layer. [5] The outer surface of the virions is studded with helical polymeric structure composed of virally-encoded and host-derived protein dimers. The virions contain at least 35 polypeptides which range in size from 10 to 200 kilodaltons.[ citation needed ]
The genome is a supercoiled, circular double stranded DNA (dsDNA) molecule ranging in size from 120 to 190 kilobases with 108-174 putative non-overlapping genes that are equally distributed over the genome in unidirectional clusters. [6] The G+C ratio varies between 28% and 44%.[ citation needed ]
Species in this family cause overt salivary gland hypertrophy symptoms in dipteran adults. Infection and replication in non-salivary gland cells induce partial in tsetse flies and complete shutdown of vitellogenesis in the houseflies,. [7] [8]
Replication occurs in the nucleus of secretory epithelial cells of the salivary gland. The viral DNA synthesis and transcription occurs within the nuclear replication complexes. Replication involved temporal expression of immediate early, early and late genes. The nucleocapsids exit the nucleus into the cytoplasm through the nuclear pore complex, after which they associate with the Golgi apparatus that culminates in cytoplasmic envelopment and virion assembly.[ citation needed ]
Transmission is either horizontally (per os) through feeding or vertically (transovarially) from mother to offspring,. [9] [10] Mechanical transmission (trans-cuticular though wounds) has been suggested in the houseflies. [11]
Two genera, each containing one species, are assigned to this family: [12]
Morphologically and symptomologically similar virus to SGHVs has been reported to cause SGH symptoms in the male accessory gland filaments of the solitary braconid wasp, Diachasmimorpha longicuadata Ashmed (Hymenoptera. Braconidae), [22] which suggests existence of other Hytrosaviridae family members.
Prevalence of this virus is high (80%) in Glossina pallidipes. Within the housefly populations, MdSGHV induces variable rates of overt SGH symptoms (0-40%), which is related to the fly's seasonal densities at various sampling sites. [23]
Hytrosaviruses (SGHVs) induce similar gross pathology (SGH symptoms) in the salivary glands of their respective adult insect hosts, but the cytopathogies are distinct for each of the two known genera (Glossinavirus and Muscavirus). Both pairs of the salivary gland tissue are equally affected (swollen up to four times their normal sizes) with the enlargement extending the entire lengths of the distal regions of the salivary glands. Infections of tissues other than the salivary glands is associated with various pathologies such as reproductive dysfunctions, infertility in females and distorted mating behaviors.[ citation needed ]
GpSGHV causes salivary gland hyperplasia in the infected tsetse flies, i.e. only the cytoplasmic but not the nuclear compartment of the glands are enlarged. [24] However, the hyperplastic salivary gland cells are capable of dividing. This pathology is thought to be due to the virus-induced reprogramming of the differentiated salivary gland cells. Overall, the induction of overt SGH symptoms is typically the exemption rather than the rule. It is only under some unknown conditions that the asymptomatic infection state is triggered to the symptomatic infection state. [25] When GpSGHV is artificially inoculated (intrahemocoelic) into adult stages of the tsetse fly Glossina pallidipes, overt SGH symptoms develop in the F1 offsprings produced by the injected mothers, but not in the parental generation. [26] MdSGHV induces salivary gland hypertrophy in the housefly, i.e. both the cytoplasmic and nuclear compartments of the salivary gland tissue proliferate, but are incapable of dividing. When MdSGHV suspensions are artificially infected into adult houseflies, the virus induces overt SGH symptoms in 100% of the infected flies within three days post infection. [27] Adult housefly develops increased resistance to MdSGHV infections with age, which is partially attributed to the development of the PM barrier in the fly's midguts.[ citation needed ]
Infections of non-salivary gland tissues in the tsetse flies by GpSGHV is associated with testicular degeneration, ovarian abnormalities, severe necrosis, degeneration of germinaria, and a reduction of the fly's development, survival and fecundity. Infections of the milk glands cause necrosis and depletion of the milk reservoir organelles.[ citation needed ]
In the housefly, MdSGHV in non-salivary gland tissues blocks the production of sesquiterpenoids, which in turn induces complete shutdown of vitellogenesis. The ovaries of viremic housefly females become arrested at the pre-vitellogenic stages. MdSGHV induces behavioral alterations in infected females, which refuse to copulate with either healthy or viremic males. [28]
The asymptomatic GpSGHV infection state represents either a sub-lethal persistence or latency. Host's RNA interference (RNAi) machineries such as the small interfering RNA (siRNA) and micro RNA (miRNA) pathways have been implicated in keeping GpSGHV infections under control,. [29] [30]
Structurally, hytrosaviruses are similar to members of other arthropod-infecting virus families such as Baculoviridae , Nudiviridae and Nimaviridae. Hytrosaviruses share 12 of the 38 core genes that have been described in baculoviruses, nudiviruses, nimaviruses and some bracoviruses. Some of the structural and genomic features shared between hytrosaviruses and other large, dsDNA viruses include the possession of enveloped, rod-shaped virions, circular dsDNA genomes and replication in the nucleus of infected cells. However, hytrosaviruses differ functionally with baculoviruses by the lack of occlusion bodies and lower lethality. [31]
The viral DNA polymerase encoded is type B, which is present and conserved in all large dsDNA viruses. At the amino acid level, the best match of the DNA polB of hytrosaviruses is to the DNA polB found in the Alcelaphine gammaherpesvirus ,. [32] [33] [34] Based on the DNA polB gene, hytrosaviruses relate more closely with invertebrate viruses with large linear dsDNA compared to viruses with circular dsDNA genomes. Some of the linear dsDNA viruses that cluster together with hytrosaviruses include members of families Herpesviridae (120-240 kp), Iridoviridae (140-303 bp), Poxviridae (130–375 kb), Phycodnaviridae (100–560 kb) and Mimiviridae (1200 kb). [35] Hytrosaviruses encode homologs to the core and highly conserved oral infectivity factor (PIF) genes found in other dsDNA viruses (PIFs o/P74, 1,2 and 3), and occlusion-derived virus (ODV) envelope of epidopteran baculoviruses (OVD-E66). Also found in hytrosaviruses are homologs to some of the subunits of the DNA-dependent RNA polymerase (DdRp) complex found in baculoviruses and nudivuses. The DdRp complex components present in the hytrosaviruses include the late expression factors 4, 5, 8 and 9 (LEF-4, LEF-5, LEF-8 and LEF-9). [36]
In mass rearing facilities, infections of tsetse flies by hytrosavirus causes reduction in colony productivity, which can cause collapse of the colonies. [37] The virus is introduced into the mass rearing facilities from asymptomatic, field-collected materials, or material derived from already existing colonies, that are used to establish new or replenish existing colonies. The virus is then spread and maintained in the colonies through vertical transmission. Unknown factors (e.g. stress or genetic) can trigger expression of overt SGH symptoms, which culminate in fly mortalities, reduced fecundity and eventual colony collapse. There are no obvious external clinical signs for hytrosavirus infections. The hytrosavirus infecting the tsetse flies can be diagnosed using a simple, sensitive and reliable non-destructive PCR-based assay, which allows the screening of the virus in individual live flies. [38] Hytrosavirus infections in mass-reared tsetse flies can be effectively managed by an integrated approach involving a "clean feeding system" (CFS), which is based on strict sanitation, regular and routing monitoring of viral infections and the occurrence of overt SGH symptoms. [39] The CFS can be combined with supplementation of bloodmeals with antiviral drugs such as valacyclovir, which are administered at low doses that are non-detrimental to the fly's DNA synthesis. [40] When administered, the antiviral drug is converted into active metabolites by the virally-encoded thymidylate synthase. The active metabolites subsequently block viral replication resulting in the reduction of viral titers and shedding.[ citation needed ]
Tsetse are large, biting flies that inhabit much of tropical Africa. Tsetse flies include all the species in the genus Glossina, which are placed in their own family, Glossinidae. The tsetse is an obligate parasite, which lives by feeding on the blood of vertebrate animals. Tsetse has been extensively studied because of their role in transmitting disease. They have a pronounced economic impact in sub-Saharan Africa as the biological vectors of trypanosomes, causing human and animal trypanosomiasis.
Trypanosomiasis or trypanosomosis is the name of several diseases in vertebrates caused by parasitic protozoan trypanosomes of the genus Trypanosoma. In humans this includes African trypanosomiasis and Chagas disease. A number of other diseases occur in other animals.
Vector control is any method to limit or eradicate the mammals, birds, insects or other arthropods which transmit disease pathogens. The most frequent type of vector control is mosquito control using a variety of strategies. Several of the "neglected tropical diseases" are spread by such vectors.
Parotitis is an inflammation of one or both parotid glands, the major salivary glands located on either side of the face, in humans. The parotid gland is the salivary gland most commonly affected by inflammation.
The adaptive immune system, also known as the acquired immune system, or specific immune system is a subsystem of the immune system that is composed of specialized, systemic cells and processes that eliminate pathogens or prevent their growth. The acquired immune system is one of the two main immunity strategies found in vertebrates.
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Trypanosoma brucei is a species of parasitic kinetoplastid belonging to the genus Trypanosoma that is present in sub-Saharan Africa. Unlike other protozoan parasites that normally infect blood and tissue cells, it is exclusively extracellular and inhabits the blood plasma and body fluids. It causes deadly vector-borne diseases: African trypanosomiasis or sleeping sickness in humans, and animal trypanosomiasis or nagana in cattle and horses. It is a species complex grouped into three subspecies: T. b. brucei, T. b. gambiense and T. b. rhodesiense. The first is a parasite of non-human mammals and causes nagana, while the latter two are zoonotic infecting both humans and animals and cause African trypanosomiasis.
Animal trypanosomiasis, also known as nagana and nagana pest, or sleeping sickness, is a disease of vertebrates. The disease is caused by trypanosomes of several species in the genus Trypanosoma such as T. brucei. T. vivax causes nagana mainly in West Africa, although it has spread to South America. The trypanosomes infect the blood of the vertebrate host, causing fever, weakness, and lethargy, which lead to weight loss and anemia; in some animals the disease is fatal unless treated. The trypanosomes are transmitted by tsetse flies.
Murine coronavirus (M-CoV) is a virus in the genus Betacoronavirus that infects mice. Belonging to the subgenus Embecovirus, murine coronavirus strains are enterotropic or polytropic. Enterotropic strains include mouse hepatitis virus (MHV) strains D, Y, RI, and DVIM, whereas polytropic strains, such as JHM and A59, primarily cause hepatitis, enteritis, and encephalitis. Murine coronavirus is an important pathogen in the laboratory mouse and the laboratory rat. It is the most studied coronavirus in animals other than humans, and has been used as an animal disease model for many virological and clinical studies.
Paratransgenesis is a technique that attempts to eliminate a pathogen from vector populations through transgenesis of a symbiont of the vector. The goal of this technique is to control vector-borne diseases. The first step is to identify proteins that prevent the vector species from transmitting the pathogen. The genes coding for these proteins are then introduced into the symbiont, so that they can be expressed in the vector. The final step in the strategy is to introduce these transgenic symbionts into vector populations in the wild. One use of this technique is to prevent mortality for humans from insect-borne diseases. Preventive methods and current controls against vector-borne diseases depend on insecticides, even though some mosquito breeds may be resistant to them. There are other ways to fully eliminate them. “Paratransgenesis focuses on utilizing genetically modified insect symbionts to express molecules within the vector that are deleterious to pathogens they transmit.” The acidic bacteria Asaia symbionts are beneficial in the normal development of mosquito larvae; however, it is unknown what Asais symbionts do to adult mosquitoes.
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The housefly is a fly of the suborder Cyclorrhapha. It possibly originated in the Middle East, and spread around the world as a commensal of humans. It is the most common fly species found in houses. Adults are gray to black, with four dark, longitudinal lines on the thorax, slightly hairy bodies, and a single pair of membranous wings. They have red eyes, set farther apart in the slightly larger female.
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Glossinavirus is a genus of viruses, in the family Hytrosaviridae. Glossina sp serve as natural hosts. There is only one species in this genus: Glossina hytrosavirus. Diseases associated with this genus include: partial sterility due to ovarian abnormalities or to testicular degeneration; can be asymptomatic in laboratory colonies.
Muscavirus is a genus of viruses, in the family Hytrosaviridae. The fly Musca domestica is the natural host. There is only one species in this genus: Musca hytrosavirus. Diseases associated with this genus include: salivary gland hypertrophy, and complete sterility of infected female flies by inhibiting eggs development.
Glossina fuscipes is a riverine fly species in the genus Glossina, which are commonly known as tsetse flies. Typically found in sub-Saharan Africa but with a small Arabian range, G. fuscipes is a regional vector of African trypanosomiasis, commonly known as sleeping sickness, that causes significant rates of morbidity and mortality among humans and livestock. Consequently, the species is among several being targeted by researchers for population control as a method for controlling the disease.
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Glossina morsitans is a species of tsetse fly in the genus Glossina. It is one of the major vectors of Trypanosoma brucei rhodesiense in African savannas.
The Sleeping Sickness Commission was a medical project established by the British Royal Society to investigate the outbreak of African sleeping sickness or African trypanosomiasis in Africa at the turn of the 20th century. The outbreak of the disease started in 1900 in Uganda, which was at the time a protectorate of the British Empire. The initial team in 1902 consisted of Aldo Castellani and George Carmichael Low, both from the London School of Hygiene and Tropical Medicine, and Cuthbert Christy, a medical officer on duty in Bombay, India. From 1903, David Bruce of the Royal Army Medical Corps and David Nunes Nabarro of the University College Hospital took over the leadership. The commission established that species of blood protozoan called Trypanosoma brucei, named after Bruce, was the causative parasite of sleeping sickness.
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