“Arbovirus” is a term for a virus transmitted to mammals by hematophagous arthropods; arboviruses; replicate in both mammals and arthropods. Since the life cycle of arboviruses is highly dependent on arthropods, control of the arthropods (vectors) is generally considered important for the control of arbovirus infection. Various pathogens that cause diseases in the medical and veterinary fields are grouped into arboviruses with a history of their discoveries since the early 20th century. Furthermore, because of recent advances in sequencing technology, new arboviruses have been discovered one after another. Here we would like to overview the known arboviruses and their infections.
African swine fever (ASF) is a hemorrhagic infectious disease of Suids, which is endemic in sub-Saharan area of African continent. ASF is usually circulating sub-symptomatically among wild species of Suidae family, such as warthogs and bush pigs, by mediating Ornithodoros soft ticks. Domestic pigs (Sus scrofa) are, however, highly sensitive to the infection and show severe clinical signs with a high mortality rate, resulting a huge impact on pork production. Currently, there is no treatment or vaccine available. The etiological agent, ASFV, is highly resistant to environmental conditions, and resides in unheated pork meat or pork meat products for a long period, which may be a chance of its long-distance spread. Since August 2018, ASFV has been circulating in East and Southeast Asian countries and may possibly be introduced into Japan. Here, I describe the outline of the disease and the etiology of the pathogen in order to remind the importance of “awareness” and “preparedness” for the disease.
Coronaviruses are pathogens that infect many of animals, resulting in respiratory or enteric diseases. Coronaviruses constitute Nidovirales together with Arteriviridae. Most of human coronaviruses are known to cause mild illness and common cold. However, an epidemic of severe acute respiratory syndrome (SARS) occurred in 2002, ten years after SARS epidemic Middle East respiratory syndrome (MERS) emerged in 2012. Now, we face on a novel coronavirus which emerges in end of 2019. This novel coronavirus is named as SARS-CoV-2. SARS-CoV-2 is spread to worldwide within one to two months and causes coronavirus disease 2019 (COVID-19), respiratory illness.
Coronaviruses are enveloped viruses possessing a positive-sense and large single stranded RNA genomes. The 5' two-thirds of the CoV genome consists of two overlapping open reading frames (ORFs 1a and 1b) that encode non-structural proteins (nsps). The other one-third of the genome consists of ORFs encoding structural proteins, including spike (S), membrane (M), envelope (E) and nucleocapsid (N) proteins, and accessory proteins. Upon infection of CoV into host cells, the translation of two precursor polyproteins, pp1a and pp1ab, occurs and these polyproteins are cleaved into 16 nsps by viral proteases. Structural proteins assemble to the vesicles located from ER to Golgi (ER Golgiintermediate compartment) and virions bud into the vesicles. Virions are released from infectedcells via exocytosis.
Coronavirus disease 2019 (COVID-19) is a respiratory tract infection caused by SARS-CoV-2. As of March 30, 2020, there have been 693,224 reported patients with COVID-19 worldwide, with 1,446 in Japan. Currently, although aspects of the route of transmission are unclear, infection by contact and by inhaling droplets is considered to be the dominant transmission route. Inflammatory symptoms in the upper respiratory tract persist for several days to 1 week after onset, and in some patients symptoms of pneumonia worsen and become severe. The presence of underlying diseases and advanced age are risk factors for increased severity. Diagnosis is based on detection of SARS-CoV-2 by polymerase chain reaction (PCR) testing of nasopharyngeal swabs or sputum. Symptomatic management is the main treatment for this disease. Although the efficacy of several agents is currently being tested, at present there is no effective therapeutic agent. To prevent infection, in addition to standard preventive measures, measures that counteract infection by contact and droplet inhalation are important. In addition, if procedures that cause aerosolization of virus are used, then measures that prevent airborne infection should be implemented.
RNA viruses do not need to take the form of DNAs, and RNAs alone complete their replication cycles. On the other hand, since the 1970s, it has been known that DNA fragments derived from RNA viruses can be detected in RNA virus-infected cells. Furthermore, in this decade, it has become clear that the eukaryotic genomes contain genetic sequences derived from non-retroviral RNA viruses. The DNA sequences derived from these RNA viruses are thought to be generatedby using a transposable mechanism of retrotransposon, such as LINE-1. Many endogenous RNA viral sequences are formed by the same mechanism as processed pseudogenes in eukaryotic cells, but the significance of the production of RNA viral "pseudogenes " in infected cells has not been elucidated. We have discovered endogenous bornavirus-like elements (EBLs), which derived from a negative-sense, single-stranded RNA virus, Bornaviruses, and have studied the evolution and function of EBLs in host animals. The analysis of EBLs provides us a clue to unravel the history of host-RNA virus coexistence. In this review, I overview about the function of endogenous RNA virus sequences, especially EBLs in mammalian genomes, and discuss the significance of endogenization of RNA viruses as viral pseudogenes in evolution.
Plant viruses, obligate parasitic pathogens, utilize a variety of host plant factors in the process of their infection due to the limited number of genes encoded in their own genomes. The genes encoding these host factors are called susceptibility genes because they are responsible for the susceptibility of plants to viruses. Plants lacking or having mutations in a susceptibility gene essential for the infection of a virus acquire resistance to the virus. Such resistance trait is called recessive resistance because of the recessive inherited characteristics. Recessive resistance is reported to account for about half of the plant viral resistance loci mapped in known cultivated crops. Eukaryotic translation initiation factor (eIF) 4E family genes are well-known susceptibility genes. Although there are many reports about eIF4E-mediated recessive resistance to plant viruses, the mechanistic insight of the resistance is still limited. Here we review focusing on studies that have elucidated the mechanism of eIF4E-mediated recessive resistance.
Productive (lytic) replication of DNA viruses elicits host cell DNA damage responses, which cause both beneficial and detrimental effects on viral replication. Viruses utilize them and selectively cancel the ‘noisy’ downstream signaling pathways, leading to maintain high S-phase CDK activities required for viral replication. To achieve this fine tuning of cellular environment, herpesviruses encode many (>70) genes in their genome, which are expressed in a strictly regulated temporal cascade (immediate-early, early, and late). Here, I introduce and discuss how Epstein-Barr virus, an oncogenic herpesvirus, hijacks the cellular environment and adapt it for the progeny production.
Productive (lytic) replication of DNA viruses elicits host cell DNA damage responses, which cause both beneficial and detrimental effects on viral replication. Viruses utilize them and selectively cancel the 'noisy' downstream signaling pathways, leading to maintain high S-phase CDK activities required for viral replication. To achieve this fine tuning of cellular environment, herpesviruses encode many (>70) genes in their genome, which are expressed in a strictly regulated temporal cascade (immediate-early, early, and late). Here, I introduce and discuss how Epstein-Barr virus, an oncogenic herpesvirus, hijacks the cellular environment and adapt it for the progeny production.
Negative-strand RNA viruses do not possess a rigid viral shell, and their structures are flexible and fragile. We have applied various electron microscopies to analyze the morphologies of influenza and Ebola virus. Our studies have revealed the native interior and exterior ultrastructures of influenza virus as well as the assembly of Ebola virus core in atomic detail.