Aichivirus A | |
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Virus classification ![]() | |
(unranked): | Virus |
Realm: | Riboviria |
Kingdom: | Orthornavirae |
Phylum: | Pisuviricota |
Class: | Pisoniviricetes |
Order: | Picornavirales |
Family: | Picornaviridae |
Genus: | Kobuvirus |
Species: | Aichivirus A |
Aichivirus A formerly Aichi virus (AiV) [1] belongs to the genus Kobuvirus in the family Picornaviridae. [2] Six species are apart of the genus Kobuvirus , Aichivirus A-F. [3] Within Aichivirus A, there are six different types including human Aichi virus, canine kobuvirus, murine kobuvirus, Kathmandu sewage kobuvirus, roller kobuvirus, and feline kobuvirus. [3] Three different genotypes are found in human Aichi virus, represented as genotype A, B, and C. [3]
AiV is a non-enveloped positive sense ssRNA virus with icosahedral morphology. [3] Aichivirus A was originally identified after a 1989 outbreak of acute gastroenteritis in the Aichi Prefecture that was linked to raw oyster consumption per genetic analysis. [1] [4] [5] Human Aichi Virus can cause gastroenteritis with symptoms arising such as vomiting, diarrhea, abdominal pain, nausea, and feve. [3] [6]
Aichivirus A can be found in a variety of environmental areas including sewage, groundwater, river water, and shellfish. [2] Aichivirus A is present in many world regions, and in sometimes greater abundance than other well-known enteric viruses. [2] Aichiviruses have been seen in Asia, Europe, South America, and Africa. [2] It has since been isolated in populations of Finnish children, [7] Pakistani children, and Japanese travelers. [8] The widespread nature of aichivirus A can be seen in the high percentage of AiV antibodies in adult human populations found in several countries. [3]
Transmission occurs through the fecal-oral route. [2] After the virus is replicated in the gastrointestinal tract, the pathogen can be found in fecal samples of infected individuals. [2] Water and shellfish contaminated with human sewage can propagate aichivirus A. [2]
Aichivirus A was first characterized after an outbreak of gastroenteritis in the Aichi Prefecture of Japan, this region is where the name of the virus was derived from. [5] Fecal samples from infected individuals were taken and transported to a lab where they described the novel virus. [5] These viral particles were 30 nm in diameter, a spherical shape, and cytopathic for BSC-1 cells (kidney cells of African green monkey). [3] [5] The infection was attributed to contaminated raw oyster found in vinegar. [5]
Aichivirus A has been seen and described across many Asian countries, however the first appearance of aichivirus outside of this region was isolated in Europe and South America in 2006. [9] Through genetic analysis of isolates from Brazil and Germany, the nucleotide sequences were found to be similar to known Aichivirus nucleotide sequences. [9] Notably, the German strain appeared to be of genotype A and the Brazil strain appeared to be of genotype B. [9] Screening in Germany for antibodies to Aichivirus displayed a seroprevalence of 76%, which is comparable to seroprevalence in Japan. [9] Therefore, European infection with Aichivirus is as common as it is in Asia. [9]
Aichivirus A enters host cells through receptor-mediated endocytosis, a cellular uptake mechanism. [3] After viral attachment and entry, the virion particle is uncoated releasing the genome into the cytoplasm. [3] Similar to other viruses within the Picornaviridae family, viral replication and translation occurs in the cytoplasm. [10] The positive sense ssRNA is directly translated into protein by the host cell ribosomes, while some of the ssRNA is used as a template to replicate the viral genome. Capsid proteins, L protein, nonstructural proteins, and stable intermediates are produced after the polyprotein is processed. Protein production is directly related to synthesis of plus-strand RNA replication complex. [10] [3] The plus-strand RNA genome is packaged into the assembled viral particle, along with VpG (Viral genomic protein). [3] A completed viral particle has 60 capsid proteins copies made up of 12 pentamers. [3] The pentamer is made up by the 5S subunit composed of VP0, VP1, and VP3 protein aggregates. [3] After the viral particle is assembled, it is released from host cells by cell lysis, making Aichivirus A a lytic virus. [3] [11]
Most aichivirus A infection in humans are mild, asymptomatic infections lasting between 48–72 hours. [3] However, it can develop into the common symptoms of gastroenteritis: fever, nausea, vomiting, abdominal pain. [12] [3] Viral replication in the gastrointestinal tract damages the enterocyte layer in the intestinal villi interfering with water reabsorption [12] This can lead to the symptoms appearing with infection.
Aichivirus A can become an opportunistic pathogen in those with HIV and is seen in high levels in the feces of those with HIV. [13] [14] Aichivirus A is also suspected as an opportunistic pathogan in those with X-linked agammaglobulinemia. [14] Aichivirus is an emerging pathogen in those with B-cell deficiencies, however there is no explanation why [14] In patients with primary immune deficiencies, chronic aichivirus infection can cause immunodysregulation. [15] Human aichivirus was deemed to effect multiple organs leading to the clinical symptom presentation. [15] The aichivirus genome was detected in symptomatic patients and in infected organs, while it was not seen in asymptomatic individuals. [15] Notably, in Japan there is a correlation with aichivirus A infection and lower respiratory tract disease. [16]
The RNA genome of AiV A is composed of 8280 nucleotides. Along the 5' end of the RNA, there is an untranslated region consisting of 744 nucleotides, a VpG protein, and an internal ribosomal entry site (IRES). Following the 5' untranslated region, the open reading frame is approximately 7.3kB consisting of 2432 amino acids. The L protein, leader peptide, is the first protein translated within the polypeptide, followed by the structural proteins, and then nonstructural proteins. Cleavage into the different proteins occurs by viral proteases. [17] The capsid proteins are made up of three segments in the RNA: VP0, VP3, and VP1. [3] [17] These capsid proteins together are known as the P1 region on the genome. [3] The encoded capsid proteins form a protomer that form into 12 pentamers during self-assembly. [17] [18] X-ray crystallography of human aichi virus virion structure determined that the VP3 knob structure and VP0 surface loop are smaller compared to other viruses in picornaviruses. [17] P2 and P3 are the regions of the RNA genome that are the non-structural proteins involved in replication control. [17] [19] For example, the protein 3D within the P3 region encodes for the viral RNA-dependent RNA polymerase used in replication. [20] The 3B protein also in the P3 region encodes for the VpG protein, which is important promoting replication. Following the P2 and P3 region, there is a 3' untranslated region of about 237 nucleotides and a poly-A tail. [3]
Differences at the 3CD nonstructural protein junction in the viral genome results in distinct genotypic differences. [21] [3] When comparing the junction between the C-terminus of the 3C region and the N-terminus of the 3D region, three distinct genotypic types are seen. [3] In studies, there appeared to be a geographical distribution to the genotypes. In some countries genotype B is prevalent, while in others genotype A dominates. In Finland and Spain genotype A was more prevalent. [7] [22] However, in China, Bangladesh, and Pakistan genotype B is more widely seen in gastroenteritis outbreaks. [23] [24] However, genotype C is not widely seen to cause human infection and has only been described in one study a fecal sample from a child case of gastroenteritis after a trip to Mali. [3] [21] The VP1 region is used to classify the picornaviruses and can also be used to differentiate between aichivirus A genotypes. [3] Some studies have seen more variation in the VP1 region and suggest that this region may be a better region to differentiate between genotypes. [9]
Aichivirus A can be found in a variety of environmental sources potentially leading to infection through food and water consumption. Aichivirus A causes infection through the fecal-oral route, where contaminated food and water sources are ingested. [3] Some studies suggest using Aichivirus A as a method to detect viral contamination in environmental samples. [2]
Enteric viruses can propagate through bivalve mollusks which filter surrounding water for food and retain enteric viruses. [3] Many safety protocols only take into account bacteria and not viruses, which makes shellfish a vector for viral transmission. [25] Aichivirus A was first detected in an outbreak due to contaminated oysters, and contaminated seafood has been associated with aichivrius A outbreaks worldwide. [3] In a year-long study in Japan on viral detection in clams, 33% of the grocery store samples contained aichivirus A. [26]
Aichivirus A has been reported at high rates in wastewater but was first seen in 2010. [27] Wastewater treatment cannot get rid of all the viral particles before being discharged into the environment. [3] Due to the stability of aichivirus in sewage before and after treatment, aichivirus A is likely a human fecal pollutant indicator. [3] Aichivirus A has been detected in wastewater in America, Europe, Africa, and Asia. [3] In one study, samples of treated sewage contained a 91.7% prevalence of aichivirus A. [28]
River water and ground water can be a reservoir for aichivirus A, due to viruses not being removed during the natural filtration cycle. [3] Aichivirus A was first studied in river water in Venezuela in 2010 with detection in 45% of samples. [27] Aichivirus A has since been detected in water sources worldwide, including in tap water and ground water in America. [3]
Under an electron microscope, Aichivirus A appears as a small, round virus making it hard to distinguish it from other viruses with a similar morphology. [16] Under electron microscopy, a canyon-like valley is seen on the surface of the capsid, likely where receptor binding occurs for entry. [3] The viral particle is stable in acidic conditions until a pH of 2 and remains stable under known experimental methods to disrupt the viral particle. [29] These methods include heat, hydrostatic pressure, and detergent conditions. [29] [3] In human cell lines like HeLa, a cytopathic effect is not seen, however a cytopathic effect is seen in BSC-1 cell lines and Vero Cells. [3]
An enzyme-linked immunoabsorbant assay (ELISA) has been developed to detect aichivirus A antigens. [16] Reverse transcription-RNA polymerase chain reaction is also widely used in aichivirus research for identification and genotype differentiation. [30] A loop-mediated isothermal amplification (LAMP) assay has been created for aichivirus A to be used in water samples. [31] The LAMP assay allows for a rapid and specific detection of aichivirus A. [31] Reverse transcription-quantitative PCR (RT-qPCR) is also widely used for detection and to determine viral numbers. [3]
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