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Virology, Epidemiology and Pathology of Glossina Hytrosavirus, and Its Control Prospects in Laboratory Colonies of the Tsetse Fly, Glossina pallidipes (Diptera; Glossinidae).

Kariithi HM, van Oers MM, Vlak JM, Vreysen MJ, Parker AG, Abd-Alla AM - Insects (2013)

Bottom Line: The sterile insect technique (SIT) is a robust control tactic that has shown to be effective in eradicating tsetse populations when integrated with other control tactics in an area-wide integrated approach.The SIT requires production of sterile male flies in large production facilities.Standard operation procedures for viral management in tsetse mass-rearing facilities are proposed and a future outlook is sketched.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Virology, Wageningen University, Droevendaalsesteeg 1, Wageningen 6708 PB, The Netherlands. henry.kariithi@wur.nl.

ABSTRACT
The Glossina hytrosavirus (family Hytrosaviridae) is a double-stranded DNA virus with rod-shaped, enveloped virions. Its 190 kbp genome encodes 160 putative open reading frames. The virus replicates in the nucleus, and acquires a fragile envelope in the cell cytoplasm. Glossina hytrosavirus was first isolated from hypertrophied salivary glands of the tsetse fly, Glossina pallidipes Austen (Diptera; Glossinidae) collected in Kenya in 1986. A certain proportion of laboratory G. pallidipes flies infected by Glossina hytrosavirus develop hypertrophied salivary glands and midgut epithelial cells, gonadal anomalies and distorted sex-ratios associated with reduced insemination rates, fecundity and lifespan. These symptoms are rare in wild tsetse populations. In East Africa, G. pallidipes is one of the most important vectors of African trypanosomosis, a debilitating zoonotic disease that afflicts 37 sub-Saharan African countries. There is a large arsenal of control tactics available to manage tsetse flies and the disease they transmit. The sterile insect technique (SIT) is a robust control tactic that has shown to be effective in eradicating tsetse populations when integrated with other control tactics in an area-wide integrated approach. The SIT requires production of sterile male flies in large production facilities. To supply sufficient numbers of sterile males for the SIT component against G. pallidipes, strategies have to be developed that enable the management of the Glossina hytrosavirus in the colonies. This review provides a historic chronology of the emergence and biogeography of Glossina hytrosavirus, and includes researches on the infectomics (defined here as the functional and structural genomics and proteomics) and pathobiology of the virus. Standard operation procedures for viral management in tsetse mass-rearing facilities are proposed and a future outlook is sketched.

No MeSH data available.


Related in: MedlinePlus

Schematic (hypothetical) representation of GpSGHV morphogenesis: (I) an enveloped (infectious) viral particle binds to receptors on susceptible host cell. (II) Once bound, the virus is uncoated as it enters the host cell (III). Cytoplasmic trafficking of the viral nucleocapsid to the nucleus ensues (IV), followed by disassembly of viral nucleocapsids by partial degradation of capsid and tegument proteins and release of viral DNA into the host cell nucleus. (V) Once in the nucleus, the virus induces formation of virogenic stroma (VS), where viral nuclear replication occurs. (VI) After packaging of nascent viral DNA into capsids, nucleocapsids are assembled, after which they egress into the cell cytoplasm. (VII) The entire envelopment of nascent nucleocapsids is orchestrated in the cytoplasm, possibly via the ER-Golgi system. (VIII) Egress of the new mature virions from the infected cell possibly occurs via rupture or disintegration of the plasma membranes.
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insects-04-00287-f004: Schematic (hypothetical) representation of GpSGHV morphogenesis: (I) an enveloped (infectious) viral particle binds to receptors on susceptible host cell. (II) Once bound, the virus is uncoated as it enters the host cell (III). Cytoplasmic trafficking of the viral nucleocapsid to the nucleus ensues (IV), followed by disassembly of viral nucleocapsids by partial degradation of capsid and tegument proteins and release of viral DNA into the host cell nucleus. (V) Once in the nucleus, the virus induces formation of virogenic stroma (VS), where viral nuclear replication occurs. (VI) After packaging of nascent viral DNA into capsids, nucleocapsids are assembled, after which they egress into the cell cytoplasm. (VII) The entire envelopment of nascent nucleocapsids is orchestrated in the cytoplasm, possibly via the ER-Golgi system. (VIII) Egress of the new mature virions from the infected cell possibly occurs via rupture or disintegration of the plasma membranes.

Mentions: The GpSGHV replicates in the nucleus of host cells, where it induces formation of virogenic stroma (chromatin-like network of electron-dense filaments) [89]. After nuclear assembly the GpSGHV progeny nucleocapsids translocate to the cytoplasm where the envelopment is orchestrated, possibly via the ER-Golgi system, based on residual ER-Golgi proteins in the virion proteome. The possibility of the ER-Golgi assembly of the tsetse virus was proposed in the 1970s [59]. Based on the GpSGHV pathobiological data obtained to date (see summary in Table 1), cytoplasmic assembly of the virus particles induces cellular damage that possibly culminates into disintegration of the cell plasma membrane as the mature virions egress from the infected cell [89]. The virions are continuously shed via the saliva into the blood meals during membrane feeding in G. pallidipes colonies, and are infectious per os to healthy flies [52,142]. A remarkable difference between GpSGHV and MdSGHV is that the MdSGHV virions migrate to, and bud out of the plasma membrane of infected cells [133,134]. Unlike GpSGHV, MdSGHV does not have surface projections. Based on the available data, an infection model for GpSGHV can be hypothesized (Figure 4).


Virology, Epidemiology and Pathology of Glossina Hytrosavirus, and Its Control Prospects in Laboratory Colonies of the Tsetse Fly, Glossina pallidipes (Diptera; Glossinidae).

Kariithi HM, van Oers MM, Vlak JM, Vreysen MJ, Parker AG, Abd-Alla AM - Insects (2013)

Schematic (hypothetical) representation of GpSGHV morphogenesis: (I) an enveloped (infectious) viral particle binds to receptors on susceptible host cell. (II) Once bound, the virus is uncoated as it enters the host cell (III). Cytoplasmic trafficking of the viral nucleocapsid to the nucleus ensues (IV), followed by disassembly of viral nucleocapsids by partial degradation of capsid and tegument proteins and release of viral DNA into the host cell nucleus. (V) Once in the nucleus, the virus induces formation of virogenic stroma (VS), where viral nuclear replication occurs. (VI) After packaging of nascent viral DNA into capsids, nucleocapsids are assembled, after which they egress into the cell cytoplasm. (VII) The entire envelopment of nascent nucleocapsids is orchestrated in the cytoplasm, possibly via the ER-Golgi system. (VIII) Egress of the new mature virions from the infected cell possibly occurs via rupture or disintegration of the plasma membranes.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4553466&req=5

insects-04-00287-f004: Schematic (hypothetical) representation of GpSGHV morphogenesis: (I) an enveloped (infectious) viral particle binds to receptors on susceptible host cell. (II) Once bound, the virus is uncoated as it enters the host cell (III). Cytoplasmic trafficking of the viral nucleocapsid to the nucleus ensues (IV), followed by disassembly of viral nucleocapsids by partial degradation of capsid and tegument proteins and release of viral DNA into the host cell nucleus. (V) Once in the nucleus, the virus induces formation of virogenic stroma (VS), where viral nuclear replication occurs. (VI) After packaging of nascent viral DNA into capsids, nucleocapsids are assembled, after which they egress into the cell cytoplasm. (VII) The entire envelopment of nascent nucleocapsids is orchestrated in the cytoplasm, possibly via the ER-Golgi system. (VIII) Egress of the new mature virions from the infected cell possibly occurs via rupture or disintegration of the plasma membranes.
Mentions: The GpSGHV replicates in the nucleus of host cells, where it induces formation of virogenic stroma (chromatin-like network of electron-dense filaments) [89]. After nuclear assembly the GpSGHV progeny nucleocapsids translocate to the cytoplasm where the envelopment is orchestrated, possibly via the ER-Golgi system, based on residual ER-Golgi proteins in the virion proteome. The possibility of the ER-Golgi assembly of the tsetse virus was proposed in the 1970s [59]. Based on the GpSGHV pathobiological data obtained to date (see summary in Table 1), cytoplasmic assembly of the virus particles induces cellular damage that possibly culminates into disintegration of the cell plasma membrane as the mature virions egress from the infected cell [89]. The virions are continuously shed via the saliva into the blood meals during membrane feeding in G. pallidipes colonies, and are infectious per os to healthy flies [52,142]. A remarkable difference between GpSGHV and MdSGHV is that the MdSGHV virions migrate to, and bud out of the plasma membrane of infected cells [133,134]. Unlike GpSGHV, MdSGHV does not have surface projections. Based on the available data, an infection model for GpSGHV can be hypothesized (Figure 4).

Bottom Line: The sterile insect technique (SIT) is a robust control tactic that has shown to be effective in eradicating tsetse populations when integrated with other control tactics in an area-wide integrated approach.The SIT requires production of sterile male flies in large production facilities.Standard operation procedures for viral management in tsetse mass-rearing facilities are proposed and a future outlook is sketched.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Virology, Wageningen University, Droevendaalsesteeg 1, Wageningen 6708 PB, The Netherlands. henry.kariithi@wur.nl.

ABSTRACT
The Glossina hytrosavirus (family Hytrosaviridae) is a double-stranded DNA virus with rod-shaped, enveloped virions. Its 190 kbp genome encodes 160 putative open reading frames. The virus replicates in the nucleus, and acquires a fragile envelope in the cell cytoplasm. Glossina hytrosavirus was first isolated from hypertrophied salivary glands of the tsetse fly, Glossina pallidipes Austen (Diptera; Glossinidae) collected in Kenya in 1986. A certain proportion of laboratory G. pallidipes flies infected by Glossina hytrosavirus develop hypertrophied salivary glands and midgut epithelial cells, gonadal anomalies and distorted sex-ratios associated with reduced insemination rates, fecundity and lifespan. These symptoms are rare in wild tsetse populations. In East Africa, G. pallidipes is one of the most important vectors of African trypanosomosis, a debilitating zoonotic disease that afflicts 37 sub-Saharan African countries. There is a large arsenal of control tactics available to manage tsetse flies and the disease they transmit. The sterile insect technique (SIT) is a robust control tactic that has shown to be effective in eradicating tsetse populations when integrated with other control tactics in an area-wide integrated approach. The SIT requires production of sterile male flies in large production facilities. To supply sufficient numbers of sterile males for the SIT component against G. pallidipes, strategies have to be developed that enable the management of the Glossina hytrosavirus in the colonies. This review provides a historic chronology of the emergence and biogeography of Glossina hytrosavirus, and includes researches on the infectomics (defined here as the functional and structural genomics and proteomics) and pathobiology of the virus. Standard operation procedures for viral management in tsetse mass-rearing facilities are proposed and a future outlook is sketched.

No MeSH data available.


Related in: MedlinePlus