ssRNA
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Single-Stranded RNA Virus
Related terms:
Enzyme
Protein
Mutation
Hepatitis C Virus
DNA
RNA
Virus Infection
Virus RNA
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Acute Viral Hepatitis
In Diagnostic Pathology: Hepatobiliary and Pancreas (Second Edition), 2017
ETIOLOGY/PATHOGENESIS
Hepatitis A Virus
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Single-stranded RNA virus in Picornaviridae family
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Usually spreads via oral or fecal-oral transmission
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Community outbreaks related to contaminated food or water
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Accounts for ∼ 1/2 of acute viral hepatitis cases in USA
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At least 4 genotypes described, but only 1 serotype exists
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Infection with one genotype confers immunity against all genotypes
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Never results in chronic infection
Hepatitis B Virus
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Partially double-stranded DNA virus in Hepadnaviridae family
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Parenteral, perinatal, and sexual transmission
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Up to 40% of acute hepatitis cases in USA attributable to hepatitis B
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∼ 10% of infected patients develop chronic infection
Hepatitis C Virus
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RNA virus of Flaviviridae family
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Parenteral, perinatal, and sexual transmission
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Accounts for ∼ 20% of cases of acute hepatitis
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Only 10-15% of infected individuals develop symptomatic acute hepatitis
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If untreated, ∼ 85% of infected patients develop chronic infection
Hepatitis D Virus (Delta Agent)
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Defective RNA virus
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Parenteral and sexual transmission
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Requires coinfection with hepatitis B virus or superinfection in patient with chronic hepatitis B virus infection
Hepatitis E Virus
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Single-stranded, nonenveloped RNA virus in Caliciviridae family
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4 routes of infection
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Vertical transmission
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Parenteral transmission
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Consumption of raw or undercooked meat of infected animals
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Contaminated water supply
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Endemic in parts of Asia, Africa, and India
Other Viruses
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CMV
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Epstein-Barr virus
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Ourmiaviruses (Ourmiavirus)
Gian Paolo Accotto, Cristina Rosa, in Reference Module in Life Sciences, 2020
Abstract
Ourmiaviruses are ssRNA viruses not assigned to any family, with a tripartite genome and cylindrical particles with conical ends. The three species described so far infect plants inducing mosaic, mottle, necrosis on the leaves: Ourmia melon virus (OuMV, the type species), Epirus cherry virus (EpCV) and Cassava virus C (CsVC). Ourmiaviruses appear derived by reassortment of genetic elements of very distant viruses. The RNA-dependent RNA polymerase (RdRp) shows relationships with viruses of invertebrates and fungi, the movement protein (MP) with tombusviruses, the coat protein (CP) shows distant affinities with the CPs of sobemo-, tombus- luteo- and nodaviruses.
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Applications of viruses for cancer therapy
Sergey A. Kaliberov, Donald J. Buchsbaum, in Advances in Cancer Research, 2012
3.3 Retroviruses/lentiviruses
Retroviruses are single-stranded RNA viruses that can integrate into the genome of cells, which results in stable replication and transmission to all the progeny of these cells. Retroviruses continue to be employed as gene delivery vehicles, although recent adverse events following retroviral gene therapy have raised concerns about potential insertional mutagenesis (Hacein-Bey-Abina et al., 2003). Lentiviral vectors can transduce both proliferating and quiescent cells. Advantages of retroviral vectors for gene therapy include potential long-term transgene expression due to integration into the target tumor cells or host genome and low immunogenicity. However, most retroviruses demonstrate low levels of transduction efficiency and only infect dividing cells during mitosis (Adamina, Daetwiler, Rosenthal, & Zajac, 2005).
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Torovirus
A.E. Hoet, M.C. Horzinek, in Encyclopedia of Virology (Third Edition), 2008
Toroviruses are single-stranded RNA viruses with a peplomer-bearing envelope that have been associated with enteric disease in cattle and possibly humans. Toroviruses appear to occur worldwide, and torovirus-like particles in fecal preparations have been reported from Europe, the Americas, Asia, New Zealand, and South Africa. These viruses have a unique C-shape or open torus morphology in the extracellular environment. There are four recognized species in the genus Torovirus (family Coronaviridae, order Nidovirales): Equine torovirus, Bovine torovirus, Human torovirus, and Porcine torovirus. Among them there is little genetic divergence (20–40%). Antigenic cross-reactivity has revealed a relationship between equine torovirus (EToV), bovine torovirus (BToV), and human torovirus (HToV). The torovirus genome contains six open reading frames (ORFs), which are transcribed as a 3′ co-terminal nested set of four mRNAs. ORF1a and -1b encode the replicase, and ORFs 2–5 encode the spike (S), membrane (M), hemagglutinin-esterase (HE), and nucleocapsid (N) proteins, respectively. EToV is apathogenic, and the only torovirus that has been grown in vitro. All BToV strains are pathogenic, causing diarrhea in experimentally or naturally infected calves. HToVs have been associated with gastroenteritis and diarrhea in children, as well as with nosocomial infections in infants with necrotizing enterocolitis.
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Lymphocytic Choriomeningitis Virus: General Features☆
R.M. Welsh, in Reference Module in Biomedical Sciences, 2014
Genetics
Like other single-stranded RNA viruses, LCMV mutates frequently, and these mutants vary in their tropism and disease-producing potential. A single passage of a cloned LCMV variant into mice will soon segregate into clear neurotropic and turbid viscerotropic plaque variants, which can be recovered from the brain and spleen, respectively. A single amino acid change in the LCMV glycoprotein (residue 260) can convert the immunostimulatory Armstrong strain of LCMV into an immunosuppressive (clone 13) variant, and these genotypes rapidly intraconvert during in vivo passage. Several strains of LCMV have been sequenced, and the highest level of sequence homology is at the 5′ and 3′ termini of the S and L virion RNA. These are presumed polymerase- binding sites well conserved throughout the arenavirus family. Different arenaviruses cross-interfere via a defective-interfering virus mechanism. The preservation of these polymerase-binding sites may allow for this heterotypic interference. The NP and GP of the Armstrong and WE strains share 90% amino acid homology.
The presence of two virion RNAs allows for high-frequency recombination due to reassortment of viral genomes. The technique of generating reassortants has led to the assignment of viral-encoded proteins to the appropriate RNA and has facilitated the mapping of genes required for disease-producing potential. The ease of producing reassortants in the laboratory suggests that they also occur in nature and probably play roles in enhancing the genetic diversity of arenaviruses.
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Etiologic Agents of Infectious Diseases
Stephanie B. Troy, Yvonne A. Maldonado, in Principles and Practice of Pediatric Infectious Diseases (Fourth Edition), 2012
Pathogen and Pathophysiology
Polioviruses are single-stranded RNA viruses belonging to the family Picornaviridae. They have a naked protein capsid with a dense central core. The capsid consists of four structural proteins, VP1, VP2, VP3, and VP4. The genomic RNA is approximately 7440 to 7500 nucleotides in length. Three serotypes of poliovirus are antigenically distinct, but all three have 70% nucleotide identity.1 Polioviruses are stable and can be stored indefinitely at −20°C and are inactivated by formaldehyde, chlorination, and ultraviolet light.
Humans are the only known natural host; however, poliovirus can replicate in other primates. The virus is exclusively propagated in cultured cells of primate origin because other cell lines lack a functional receptor molecule. Since identification and molecular cloning of the viral receptor, transgenic mice have been developed that are susceptible to all three serotypes of poliovirus.2
Poliovirus is transmitted primarily by the fecal–oral route and replicates in the pharynx and lower intestinal tract (Table 235-1). Only small amounts of infectious virus are needed to cause infection. Virus is shed in the pharynx for 1 to 3 weeks and in the gut for 4 to 8 weeks after primary infection. During reinfection, pharyngeal shedding is rare and fecal shedding is reduced to less than 3 weeks. The incubation period generally is 7 to 14 days but can be as short as 3 days and as long as 35 days. The virus spreads quickly from the alimentary tract to regional lymph nodes. After several days, a minor viremia ensues, and a number of sites, such as muscle, fat, liver, spleen, and bone marrow, become infected. If virus is contained at this point, subclinical infection occurs. Further replication of virus in these tissues leads to major viremia and the onset of clinical symptoms. The central nervous system (CNS) is seeded during the viremic phase in approximately 1% of infections. The virus can also infect the CNS via axonal transport from skeletal muscle;3 such infection may correlate with the intense myalgia seen at the onset of paralysis in affected individuals.
Poliovirus replicates within neurons; the anterior horn cells of the spinal cord are involved most often. Neurons in nuclei of the medulla, vermis of the cerebellum, midbrain, thalamus and hypothalamus, palladium, and motor cortex of the cerebrum also can be involved. Rarely, the posterior horn cells and dorsal root ganglia are infected. Although poliovirus infection usually destroys neurons, injury occasionally is reversible.
Serum neutralizing antibody develops after about 1 week and protects against paralysis but not reinfection. Immunity to poliovirus infection is type specific, without any cross-protection, and persists for life. Local antibody appears 1 to 3 weeks after infection and limits virus replication at the mucosal level. Reinfection occurs; however, the duration of shedding is reduced and viremia does not occur. Immunodeficient individuals are at considerable risk of disseminated infection.
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Immunity to Pathogens and Tumors
Alan Rickinson, ... Martin Rowe, in Encyclopedia of Immunobiology, 2016
Human T Lymphotropic Virus-1
Retroviruses, single-stranded RNA viruses with the capacity for reverse transcription into DNA, are another virus family whose oncogenic potential was initially recognized through pioneering studies in animal systems. Interestingly the first human retrovirus, the human T lymphotropic virus-1 (HTLV1) discovered in 1980 (Poiesz et al., 1980), remains the only such agent directly linked to malignancy in man. HTLV1 is rare in many human populations but is more common in certain parts of Japan, equatorial Africa, the Caribbean, and South America, where 2–3% infected individuals eventually go on to develop a distinct adult T cell leukemia/lymphoma (ATL) and a slightly lower number suffer inflammatory disorders, particularly a chronic progressive myelopathy (Matsuoka and Jeang, 2007; Tattermusch and Bangham, 2012; Cook et al., 2013).
HTLV1 preferentially infects T cells, most often the CD4+ subset, and is transmitted not as a free virus but within latently infected T cells present in breast milk, semen, or blood. After transmission, such cells activate to produce infectious virions which then enter host T cells either through tight T cell–T cell synapses or via dendritic cell surfaces as an intermediary (Matsuoka and Yasunaga, 2013). As with all retroviruses, the RNA genome is then reverse-transcribed to a double-stranded DNA proviral copy that integrates into the cellular genome and acts as a permanent template for viral RNA synthesis. HTLV1 is a complex retrovirus which, besides the standard virion components (gag, pol, env), encodes six regulatory and/or accessory proteins. Of these, the key players are the transcriptional activator Tax and its regulator HBZ, which together drive the clonal proliferation of latently infected cells in vivo (Matsuoka and Yasunaga, 2013). This strategy (Figure 2) allows the virus to first enter and then colonize the naïve host as a cell-associated latent infection, against which neutralizing antibodies (whether induced by infection or by vaccination) would offer little defense.

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Figure 2. Human T lymphotropic virus-1 (HTLV1) infection and HTLV1-associated tumorigenesis from an immunological perspective. Initial infection occurs through transmission of latently infected T cells (either in blood or breast milk) from an HTLV1-positive donor. Virus particles produced by donor cell reactivation then gain access to host T cells, leading to a growth-transforming latent infection that is kept in check by HBZ- and/or Tax-specific CD8+ T cells. A stable virus–host equilibrium is reached with multiple HTLV1-positive T cell clones detectable in the blood of asymptomatic virus carriers. Nevertheless, growth-transforming infections continue to challenge the immune system, and over time, additional cellular genetic changes (often accompanied by downregulation of the immunodominant antigen Tax) allow an individual T cell clone to become dominant. Ultimately such a clone can progress to a fully malignant T cell lymphoma, particularly in circumstances where HTLV1-specific T cell surveillance is weak.
Turning to cell-mediated immune responses, natural killer (NK) cells also appear unable to recognize latently infected targets, whereas there is compelling evidence of an important role for T cells (Rowan and Bangham, 2012; Cook et al., 2013). First, several reports describe rapid progression to high proviral loads/ATL in HTLV1-infected patients receiving T cell–suppressive drugs. Second, in asymptomatic virus carriers there is a clear inverse relationship between proviral load (i.e., the number of HTLV1-infected cells) in the blood and the strength of the virus-specific CD8+ T cell response as measured in ex vivo functional assays. Third, certain HLA class I alleles found to protect against progressive HTLV1 infection/inflammatory disease also show the most avid binding of HBZ peptides recognized by CD8+ T cells. This chimes with the idea that, although the memory CD8 response to Tax is numerically dominant in the blood of asymptomatic carriers, the HBZ response may be just as important in determining the long-term viral load in vivo (Cook et al., 2013).
While multiple HTLV1-positive T cell clones each with unique proviral integration points are detectable in the blood during asymptomatic virus carriage, progression to full-blown ATL involves the evolution of a single malignant clone (Bangham et al., 2014). The details of that evolution, and the virus' contribution to malignant growth, are still not fully understood. However, while the proviral Tax gene is often inactivated by mutation or hypermethylation and only around 30% of ATLs continue to express the protein, HBZ is always present and likely contributes both to growth and the tumor's antiinflammatory, Th2-like, phenotype (Sugata et al., 2012). Yet such HBZ (Tax)-expressing cells remain potentially antigenic, and the fact that HTLV1-specific CD8 responses are weak in ATL patients compared to asymptomatic controls suggests that impaired T cell surveillance remains an important factor favoring tumor development (Rowan and Bangham, 2012).
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