Abbreviations : Report Help
Members of the genus Glossinavirus can switch from an asymptomatic infection to the occasional state of symptomatic infection which elicits salivary gland hypertrophy syndrome (SGH) epizootics that reduce fly fecundity and cause colony collapse (Abd-Alla et al., 2011). Intra-hemocoelic injections of glossinavirus into larvae or adults does not induce overt SGH in the same fly generation, rather, the symptoms occur in the F1 progeny (Boucias et al., 2013b, Demirbas-Uzel et al., 2018). Transmission of glossinavirus occurs both horizontally (fly-to-fly via SG secretions) and vertically (mother-to-offspring either transovarial or via milk gland secretions) (Abd-Alla et al., 2010, Boucias et al., 2013b). Viremic flies are partially sterile due to gonadal lesions and ovarian abnormalities caused by the virus (Abd-Alla et al., 2011).
Virions are long, rigid, rod-shaped particles (approximately 50–65 nm in width and 1000 nm in length) and consist of an electron-dense helical nucleocapsid core (40 nm in diameter) surrounded by a proteinaceous tegument matrix (10 nm thick) encapsulated by an outer lipid bilayer envelope presumably containing viral glycoproteins (Figure 1A.Hytrosaviridae) (Kariithi et al., 2013b, Orlov et al., 2018). The asymmetric virions have one rounded end and one conical (Orlov et al., 2018) (Figure 1C.Hytrosaviridae and 1D.Hytrosaviridae). The outer surface of the virion is studded with left-handed helical polymeric spikes (13 nm long; 15 nm periodicity) composed of virus and host-derived protein dimers (23 spikes × 24 helical turns = 1104 envelope dimers) (Kariithi et al., 2013b, Orlov et al., 2018).
Particles have a density of 1.153 g cm-3 in Nycodenz (Kariithi et al., 2010). Virions are fragile and the envelope can be detached by treatment with common buffers (Kariithi et al., 2013b, Orlov et al., 2018, Kariithi et al., 2010).
The glossinavirus genome is a circular dsDNA molecule (Abd-Alla et al., 2008, Abd-Alla et al., 2016) that encodes homologues of 12 of the 38 so-called core genes of baculoviruses and nudiviruses that are involved in: (i) DNA replication/replication (e.g. DNA polymerase, helicases); (ii) transcription (e.g. late effector factors; LEFs); (iii) packaging, assembly and release; (iv) cell cycle arrest and /or interactions with host proteins (e.g. desmoplakin and Ac81); and (v) oral infectivity (e.g. per os infectivity factors; PIFs) (Kariithi et al., 2013b, Abd-Alla et al., 2016).
Transcriptome and proteomic analyses provide evidence that 61 of the glossinavirus ORFs are translated into virus proteins (Kariithi et al., 2013b, Kariithi et al., 2010, Abd-Alla et al., 2016). At least 45 of these proteins are virion structural proteins, of which 10, 15 and 20 are associated with the envelope, nucleocapsid and in the tegument components of the virions, respectively (Kariithi et al., 2013b). Additionally, the virion proteome also contains 51 host-derived proteins, some of which are incorporated into the tegument matrix, where they may play specific or auxiliary roles in the virus replication cycle (Kariithi et al., 2013b).
The virion envelope that encapsulates the tegument is composed of a lipid bilayer (Kariithi et al., 2013b, Orlov et al., 2018) but its composition is unknown.
The virion envelope and tegument potentially contain virus proteins that include NXT motifs, as well as host-derived glycoproteins acquired from the host during the cytoplasmic envelopment process of the virus (Kariithi et al., 2013b, Orlov et al., 2018).
The genomes of the Ugandan and Ethiopian glossinavirus strains have 190,032 and 190,291 bp (28% and 27.9% G+C content) respectively, encoding 160 and 174 putative non-overlapping genes that are evenly distributed over both DNA strands in unidirectional clusters (Abd-Alla et al., 2008, Abd-Alla et al., 2016). Of the glossinavirus ORFs, ~ 90%, 84% and 36% contain TATA-like box elements, polyadenylation signals and canonical baculovirus late (T/G/A)TAAG transcriptional initiation motifs, respectively (Abd-Alla et al., 2016). Approximately 3% of the glossinavirus genome is composed of head-to-tail tandem repeat sequences, which are thought to serve as regulators of gene expression and/or origins of DNA replication (Abd-Alla et al., 2008, Abd-Alla et al., 2016). Fifty-seven genes encode structural virion proteins, while 12 genes encode non-structural proteins (Kariithi et al., 2013b, Abd-Alla et al., 2016). Glossinavirus capsids assemble in the nucleus of infected cells and are thought to acquire bilayer lipidic envelope after moving through the nuclear pores and budding through the endoplasmic/Golgi membranes (Kariithi et al., 2013b).
Members of the genus Glossinavirus are currently restricted to the hematophagous tsetse flies (Glossina species). Virus infection reduces fecundity, sometimes resulting in the collapse of laboratory colonies of some tsetse species such as Glossina pallidipes (Abd-Alla et al., 2010). Tsetse flies are not highly susceptible to glossinavirus infection; injection of millions of glossinavirus virions results in only a small fraction of the injected flies developing SGH (Boucias et al., 2013b, Demirbas-Uzel et al., 2018). There is no available cell culture systems capable of supporting glossinavirus replication (Arif and Pavlik 2013).
Tsetse flies are the natural (currently the only known) hosts for members of the genus Glossinavirus; infections can either be chronically asymptomatic or cause severe and acute symptomatic SGH syndrome (Abd-Alla et al., 2010). Members of the genus Glossinavirus are highly specific to Glossina species and are not known to induce overt SGH in heterologous hosts such as housefly (Abd-Alla et al., 2011, Boucias et al., 2013b). The susceptibility of tsetse flies to glossinavirus infections varies widely amongst different Glossina species; G. pallidipes is the most susceptible (Demirbas-Uzel et al., 2018). There is genetic spatial variation among glossinavirus isolates from different Glossina species (Kariithi et al., 2013a, Meki et al., 2018).
Virus transmission is both horizontal (fly-to-fly) via salivary gland secretions and vertical (mother-offspring) via milk gland secretions and trans-ovarially (Abd-Alla et al., 2010, Abd-Alla et al., 2011, Boucias et al., 2013b). There is no evidence for mechanical transmission of glossinavirus. The solitary nature of the tsetse fly host is compatible with vertical transmission of glossinavirus in the field.
The specificity of glossinavirus to Glossina species restricts the geographical distribution of the virus in regions where tsetse flies occur, i.e. sub-Saharan Africa countries (Kariithi et al., 2013a, Meki et al., 2018).
Glossinavirus-induced SGH (Figure 4C.Hytrosaviridae) is associated with testicular degeneration, ovarian abnormalities, compromised development, survival, fertility and fecundity of infected tsetse flies (Abd-Alla et al., 2010). Virus infection affects sperm production and avidity of tsetse males and causes partial sterility in females (Mutika et al., 2012). Overt SGH symptoms are more prevalent in G. pallidipes, and even in this species, overt SGH symptoms are an exception rather than the rule; the factors that trigger the switch from asymptomatic to symptomatic infection states are unknown (Abd-Alla et al., 2010, Abd-Alla et al., 2011, Demirbas-Uzel et al., 2018, Kariithi et al., 2013a, Abd-Alla et al., 2013). Glossinavirus-infected SGs contain layers of dividing cells, which result in hyperplasia; in part due to cell proliferation responses resulting from virus reprogramming of the differentiated gland cells (Figure 4D.Hytrosaviridae) (Kariithi et al., 2013b, Kariithi et al., 2017a). Virus replication in other cells such as the tracheal cells and milk glands can also result in extensive hypertrophy, but without hyperplasia. Artificial injection of virus suspensions into adult flies does not result in overt SGH symptoms in the same (parental) generation, but rather in the F1 progeny, implying that the injected virus is unable to reach and replicate in fully differentiated SGs of adult flies (Boucias et al., 2013b, Demirbas-Uzel et al., 2018).
No demarcation criteria are defined yet since there is only a single species (Glossina hytrovirus) in this genus. Two lineages of the species can be demarcated based on differences in gene contents (nucleotide and deduced amino acid data), pathogenicity in different G. pallidipes sub-populations (Abd-Alla et al., 2016), and possibly host eco-geography (Kariithi et al., 2013a, Meki et al., 2018).
Support for preparation of the Online Report and Report Summaries has been provided by: