The advantageous and deleterious mutations often show complex epistatic interactions that likely have major effects on the rate and progress of adaptation. As one example, in the case of vesicular stomatitis virus, regaining full fitness after host transfer is a complex process involving multiple compensatory changes An important constraint influencing emergence and successful host transfer is the mode of virus transmission. For example, arthropod vectors that feed on a range of mammalian hosts can facilitate cross-species viral exposures. However, both phylogenetic and in vitro studies of arboviruses indicate that their levels of variation are relatively constrained compared to what is observed for viruses transmitted by other mechanisms 62 , , , Those viruses would need to balance the fitness in at least three hosts during the process of adaptation, i.
Adaptation to interhost transmission by droplet spread, that by sexual inoculation, and that by fecal-oral transmission each represent different adaptational challenges due to host differences and variation in environmental exposure. However little is known about how shedding and infection are controlled in different hosts. For example, it is not clear why influenza A viruses are enteric viruses in their natural avian hosts but mainly infect the respiratory tract in mammals, but this likely influences the host adaptation of the viruses to mammals and the ability to spread efficiently.
For many viruses, recombination and its variation seen for viruses with segmented genomes, reassortment allow the acquisition of multiple genetic changes in a single step and can combine genetic information to produce advantageous genotypes or remove deleterious mutations. Examples of reassortment in disease emergence include the emergence of the H2N2 and H3N2 influenza A pandemic viruses, where new avian genome segments were imported into the backbone of descended H1N1 viruses , as well as the emergence of the pathogenic Fujian H3N2 influenza strain by interclade reassortment Aside from segmental reassortment, recombination is rare among negative-stranded RNA viruses, while retroviruses such as HIV have high rates of recombination 20 , 52 , Recombination between viruses from different primate hosts was associated with human HIV emergence; the possible donor host origins, recombination events, and intermediate host transfers are depicted in Fig.
The SARS CoV appears to have arisen from a recombinant between a bat CoV and another virus most likely also a bat virus before infecting humans and carnivore hosts Fig. As described above, part of the receptor binding sequence of this virus may have been acquired by recombination with a group 1 human CoV, which was then selected for more-efficient use of the human ACE2 receptor Fig.
Origins of HIV-1 in humans from related viruses in chimpanzees, possible pathways of origin from other primates, and the possible roles of recombination. Cartoons showing three possible alternative routes of cross-species transmissions giving rise to chimpanzee SIV SIVcpz as a recombinant of different monkey-derived SIVs illustrate the possible complexity of the steps leading to the introduction of viruses into a new host. A Pan troglodytes troglodytes as the intermediate host. Chimpanzees have not been found to be infected by these viruses.
C Transfer through an intermediate host yet to be identified that is the current reservoir of introductions of SIVcpz into current communities of P. Reprinted from reference 40 with permission of AAAS. The blue and red horizontal arrows represent the essential ORFs from the major and minor parents, respectively. The black vertical arrow below the alignment indicates the estimated breakpoint located immediately after the start codon of the S coding region.
Reprinted from reference 44 with permission. Many recombinations or reassortments are likely to be deleterious in that they disrupt optimal protein structures or functional gene combinations. The HA and NA proteins of influenza A viruses both act on the cell's sialic acid receptors, and complementarity between virus binding HA and cleavage NA activities is often required for optimal binding to and release from cells expressing different glycan receptors , , Amino acid residues that distinguish human and avian influenza virus polymerases identified by comparison of the genome of the human virus strain with those of other human, avian, swine, and equine viruses a.
Recombination and reassortment may also be important for incremental host adaptation after switching to the new host has occurred. For example, after the emergence of human H3N2 influenza virus, which contained HA and PB1 gene segments imported from avian viruses, extensive secondary reassortments occurred after transfer, which may have facilitated its further adaptation The process of virus transfer to a new host is rarely observed directly but can be inferred by comparing viral ancestors in donor hosts with emergent viruses from recipient hosts.
If several changes are required to allow host switching, then intermediate viruses would likely be less fit in either the donor or recipient hosts than the parental or descendant viruses 60 Fig.
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As mentioned previously, influenza A reassortant viruses carrying single genomic segments from viruses of alternative hosts showed replication in either of those hosts that was lower than that seen for the parental viruses in their original hosts. The adaptation of FPV to dogs also occurred through at least one lower-fitness intermediate, as the first viruses collected from dogs were both less fit in cats than the FPV from which they were derived and less well adapted in dogs than the CPV variants that replaced them , Evolutionary models and examples of cross-species transmission of viruses.
A Here the donor and recipient species represent two distinct fitness peaks for the virus which are separated by a steep fitness valley. Multiple adaptive mutations circles are therefore required for the virus to successfully replicate and establish onward transmission in the recipient host species. B The donor and recipient species are separated by a far shallower fitness valley. This facilitates successful cross-species transmission because only a small number of advantageous mutations are required. C The emergence of CPV as an example of multiple mutations being required for a virus to adapt to a new host, after which the virus evolves within the recipient species.
The phylogeny of the capsid protein gene shows only a single origin of all the CPVs. In this example, there were two known host range adaptation steps where there were multiple mutations indicated by circles. D A second form of host transfer, where there is a lower evolutionary barrier to cross-species transfer, allowed the establishment of the different HIV clades in humans, suggesting a lower barrier to transfer into the new host species. Adapted from reference 55 with permission of AAAS. If the transmission rate in the new host population allows virus maintenance, then the length of the period of lower replication and spread would be a function of the number of genetic changes required to gain high transmissibility.
Early detection of inefficiently spreading viruses in a new host would provide opportunities for epidemic control. In the SARS CoV outbreak, the first virus that emerged was only inefficiently transmitted by most infected people, and early recognition of the outbreak and institution of active control measures particularly quarantine allowed the epidemic to be stopped before the virus could become fully established in humans 4 , , Fig.
In addition to optimizing replicative efficiency in cells and tissues, a new virus may have to optimize the intensity of viral shedding from appropriate sites for transmission e. As described above, this process likely requires adaptation to allow passage through host-specific passive barriers at the mucosal surfaces and to avoid early elimination by innate immune responses , SARS as an example of the global spread of a respiratory virus in humans after transfer from a zoonotic reservoir.
The time line is of the SARS coronavirus global outbreak from the initial human infections in China in late to the global spread of the virus and the subsequent control of the spread of the virus in mid Numbers indicate the total number of confirmed cases in each country.
Adapted from reference 33 with permission. During the early stages of an outbreak, infected individuals who cause a large number of new infections may play a critical amplifying role.
Animal-to-animal or person-to-person transmission has been a difficult subject to investigate experimentally, and we know relatively little about the specific factors that control it for most viruses, particularly during transfers into new hosts. Detailed pathogenesis studies in experimental animals will be required to achieve a better understanding of these factors. For many host-switching viruses, full host adaptation may take months or even years to complete. The SARS CoV appeared to gain some host-adaptive changes during its spread among humans, suggesting that it was on the path to full human adaptation 71 , Fig.
Isolates of Nipah virus collected at the end of the outbreak also differed significantly from those collected at the beginning, suggesting either adaptation 1 or possibly the occurrence of more than one introduction Adaptation of one HA gene during the spread of the avian influenza A viruses among different avian species and populations a. The coordination of functions under multiple selections is seen for a number of emerging viruses, as described above for selections of the HA and NA functions or polymerase subunits of influenza viruses in new hosts 36 , 48 , Some receptor binding sites are also antigenic sites on the viral proteins.
For CPV and SARS CoV, changing the binding sites for receptors also altered the antigenic structure of the virus, suggesting that there would be synergistic or competitive effects on the virus in an immune population 45 , 70 , Considerable progress has been made in identifying the many factors that control or influence virus host switching.
While it is still not possible to identify which among the thousands of viruses in wild or domestic animals will emerge in humans or exactly where and when the next emerging zoonotic viruses will originate, studies point to common pathways and suggest preventive strategies. With better information about the origins of new viruses, it may be possible to identify and control potentially emergent viruses in their natural reservoirs.
Conventional infection control procedures such as health monitoring and quarantine can substantially reduce contact between reservoir and recipient hosts, preventing outbreaks or terminating them after host transfer but while they are still limited in size For arboviruses, vector control can limit the transmission of viruses from their reservoirs to new hosts.
There is arguable evidence that public health measures undertaken in were effective in controlling the influenza pandemic of that year 8 , Vaccination has been used successfully for partial control of rabies in the United States and Europe by vaccinating raccoons or foxes and for control of wild dog rabies in Kenya and Tanzania by vaccinating domestic dogs. Therefore, coordinated strategic planning is critical for the rapid responses required to confront new viruses early after emergence. Such planning must be somewhat generic because we lack the ability to predict which virus will emerge or what its pathogenic or transmission properties will be.
National and international planning is also critical, including the harnessing of scientific and diagnostic technologies and establishing methods for rapidly communicating information about outbreaks and for coordinating control measures. Preemptive strategies should include improved surveillance targeted to regions of high likelihood for disease emergence, improved detection of pathogens in reservoirs or early in outbreaks, broadly based research to clarify the important steps that favor emergence, and modified forms of classical quarantine or other control measures.
Human disease surveillance clearly must be associated with enhanced longitudinal veterinary and wild-animal infection surveillance 28 , Vaccine strategies could be used in some control programs, but the current rate of development and approval of human vaccines is too low to allow control of most newly emerging virus diseases. Existing vaccines can be used to control the emergence of known viruses when sufficient lead time is available, as might veterinary vaccines which can be developed relatively quickly and used to combat outbreaks, along with the culling or quarantine measures that are now often used.
New and improved vaccine technologies include molecularly cloned attenuated viruses that can be rapidly changed into the appropriate antigenic forms with sufficient efficacy and a level of risk low enough for use in the face of some outbreaks. Antiviral drugs may be used where available, although cost, logistic problems, and side effects may make those more difficult to use in a large-scale outbreak, and they would likely work only in the context of other control measures 25 , The emergence of new viral diseases by animal-to-human host switching has been, and will likely continue to be, a major source of new human infectious diseases.
A better understanding of the many complex variables that underlie such emergences is of utmost importance to public health. National Institutes of Health. National Center for Biotechnology Information , U. Microbiol Mol Biol Rev. Holmes , 2 David M. Burke , 5 Charles H. Calisher , 6 Catherine A. Laughlin , 4 Linda J. Saif , 7 and Peter Daszak 8. Author information Copyright and License information Disclaimer.
This article has been cited by other articles in PMC. Open in a separate window. Time not known; after the establishment of populations sufficient to allow transmission Smallpox virus Other primates or camels? Humans Host switching and adaptation? Influenza virus Water birds Humans, pigs, horses Host switching and adaptation, possible role of intermediate host; many examples. Reassortment involved in and emergences. Earlier epidemic viruses not characterized. Changes in several genes required for success in new host CPV Cats or similar carnivores Dogs Host switching and adaptation; several mutations in the capsid control binding to the canine transferrin receptor.
Nipah virus Fruit bats Humans via pigs, or direct bat-to-human contact Host switching; adaptation may not be necessary: Chimpanzees and humans Host switching; adaptation not certain Myxoma virus Brush rabbits and Brazilian rabbits European rabbits Existing host range, required contact; spread widely in s by human actions; high virulence, adaptation after host emergence Hendra virus Fruit bats Horses and humans Host switching; adaptation not reported Canine influenza virus Horses Dogs Host switching; adaptation to dog may be occurring.
Influenza A virus subtype Location of outbreak Year of outbreak No.
Emerging animal viruses: real threats or simple bystanders?
Ecology and Contact with Alternative Hosts Contact between donor and recipient hosts is a precondition for virus transfer and is therefore affected by the geographical, ecological, and behavioral separation of the donor and recipient hosts. The Role of Host Genetic Separation Spillover or epidemic infections have occurred between hosts that are closely or distantly related, and no rule appears to predict the susceptibility of a new host.
Host Tissue Specificity and External Barriers in Alternative Hosts An initial level of protection of hosts against viruses occurs at the level of viral entry into the skin or mucosal surfaces or within the blood or lymphatic circulation or tissues. Receptor Binding The initial viral interaction with cells of a new host is a critical step in determining host specificity, and changes in receptor binding often play a role in host transfer. Intracellular Host Range Restrictions After receptor binding, restriction may also occur at other levels in viral infection cycles.
Adapted from reference 79 with permission from Macmillan Publishers Ltd. Viral Fitness Trade-Offs A fundamental challenge for host-switching viruses that require adaptation to their new hosts is that mutations that optimize the ability of a virus to infect a new host will likely reduce its fitness in the donor host Fig. Mode of Virus Transmission An important constraint influencing emergence and successful host transfer is the mode of virus transmission.
Recombination and Reassortment in Viral Evolution Leading to Host Switching For many viruses, recombination and its variation seen for viruses with segmented genomes, reassortment allow the acquisition of multiple genetic changes in a single step and can combine genetic information to produce advantageous genotypes or remove deleterious mutations. Adapted from reference with permission from Elsevier. Sites are numbered from the beginning of the mature H5 HA1 protein.
Isolation and molecular identification of Nipah virus from pigs. December , posting date. The role of evolution in the emergence of infectious diseases.
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Dynamically modeling SARS and other newly emerging respiratory illnesses: Requirements for species-specific papovavirus DNA replication. The effect of public health measures on the influenza pandemic in U. Phylogenetic analysis of the Arenaviridae: The evolution of H5N1 influenza viruses in ducks in southern China. Viral load distribution in SARS outbreak.
Cross-Species Virus Transmission and the Emergence of New Epidemic Diseases
Diseases of humans and their domestic mammals: However, in both events there was no evidence of horizontal transmission among dogs. As the H3N8 CIV is a relatively novel pathogen in the canine population, dogs lack natural immunity against the virus. Thus, all dogs, regardless breed or age, are susceptible to H3N8 CIV infection and the virus rapidly spreads within dog populations.
Additionally, stressful situations, - such as travel, prolonged endurance exercise in severe weather, and exposure to harsh terrain -, might increase the risk for influenza infection in dogs Pecoraro et al. CIV infection is not considered a seasonal flu and dog infections can occur year-round Crawford et al. The presence of all eight CIV genes of equine origin indicates transmission of the whole virus from horses to dogs, without reassortment events Crawford et al. Evidences to date support that the spillover resulted from a single event of virus transmission with subsequent adaptation to the new host.
CIV is transmitted by direct contact, through aerosols generated by coughing and sneezing and by indirect contact through fomites contaminated with respiratory secretions and by people handling septic animals Crawford et al. The incubation period is usually less than five days, with the highest shedding occurring before the development of clinical signs Crawford et al. CIV replicates in the respiratory epithelium, causing tracheitis, bronchitis and bronchiolitis Crawford et al. As a result, the defense mechanisms of the respiratory tract become severely compromised, predisposing to secondary infections by bacteria or mycoplasma.
Dogs of all ages seem to be equally susceptible to CIV-associate pneumonia Dubovi The cough is usually non-productive and persists for 10 to 30 days. Most dogs eradicate the infection and recover clinically within two weeks Beeler , Dubovi As the clinical disease associated with CIV infection is similar to that observed in "kennel cough" or infectious tracheobronchitis, CI diagnosis requires laboratory confirmation Mochizuki et al. Treatment consists mainly of supportive care, including antibiotics for secondary bacterial infections and hydration Beeler Preventive measures include isolation of sick dogs and decontamination of premises with quaternary ammonium or sodium hypochlorite.
Contact of horses with dogs should be avoided during outbreaks of equine influenza Beeler Vaccination of dogs against H3N8 CIV has been authorized in the USA since , but vaccination should be restricted to animals that travel to high-risk areas experiencing canine or equine influenza Deshpande et al. Vaccination significantly reduces virus shedding and the severity and duration of clinical disease, including the incidence and severity of lung damage Deshpande et al.
Despite description of occasional outbreaks in USA, the current incidence trends remain unclear Hayward et al. The genus Pestivirus, family Flaviviridae, is composed by four important pathogens of livestock: The pestivirus genome is composed by a positive single stranded RNA molecule around The 5'UTR region is highly conserved among pestiviruses and the comparison of this region is widely accepted for phylogenetic analysis as well as the comparison of sequences coding for the viral proteins N pro , Erns and E2.
In addition to the recognized species, four proposed Pestivirus species remain officially unrecognized Fig. Hobi-like viruses are related to BVDV at the genetic and antigenic levels. Further, the disease caused by these new viruses resembles the clinical presentations historically associated with BVDV infection, including decrease in circulating white blood cells, growth retardation, respiratory disease, reduced reproductive performance, and increased mortality among young stock Cortez et al.
Likewise, both BVDV killed or modified live vaccines seem to induce weak cross protection to Hobi-like viruses Bauermann et al. This low cross-reactivity may be translated into a high number of animals unprotected against infection, shedding and generation of persistently infected calves. Due to reports of Hobi-like virus in Brazilian cattle herds, and description of contaminated Brazilian FBS, it is assumed that Hobi-like viruses are widespread in Brazilian herds Cortez et al. Nevertheless, reports of Hobi-like virus in cattle herds in Southeast Asia and Europe demonstrated that these viruses are not restricted to South America Decaro et al.
The origin of Hobi-like viruses is unclear. One hypothesis is that these viruses originated in South America and then were introduced to other countries through contaminated biological products. Also, the ability of pestiviruses to infect other species than the primary host may explain the emergence of Hobi-like viruses in cattle.
One of the first Hobi isolates BrazBuf9, reported by Stalder et al. Regardless whether Hobi-like virus was originated in other species than cattle, current data support that the virus is well adapted and widespread in cattle populations. The first evidence of Hobi-like virus infections in Brazilian herds came from Cortez et al. Additional evidence of the circulation of the virus in the country was reported by Bianchi et al. One isolate was identified in commercial frozen semen sample following description of blindness in newborn calves in herds using this semen.
Two other viruses were identified in samples from herds with history of reproductive failure in Southern Brazil. An epidemiological study demonstrated that animals in four herds seroconverted to Hobi-like viruses, although no clinical signs were observed. Using heat inactivated serum samples, one calf was identified as positive for Hobi-like virus using antigen capture enzyme linked immunosorbent assay ACE. Later in Italy, , Hobi-like virus emerged in an outbreak of respiratory disease affecting 26 calves aging 6 to 7 months-old Decaro et al.
Hobi-like virus was detected by qRT-PCR in nasal discharge samples of six calves and in the lungs of the two dead animals. The clinical signs included fever Experimental infection of calves with Hobi-like virus leads to unapparent to mild clinical signs including increased body temperature and decreased white blood cell levels Schirrmeier et al. On one hand, some BVDV assays as ACE are able to detected Hobi-like virus, on the other hand, the sensitivity of pair of primers known so far as "panpestiviruses" may lead to elevate number of false negative results Bauermann et al.
Moreover, indicative information whether herds were exposed to different bovine pestiviruses may be achieved by analyses of the serologic response when comparing the antibody neutralizing titers of the serum against BVDV1, BVDV2, and Hobi virus Bauermann et al. On the other hand, the use of BVDV antibody detection ELISA kits for detection of animals exposed to Hobi-like viruses may generate high levels of false negative results, and the detection of positive samples is usually delayed 1 to 2 weeks when comparing with virus-neutralization test detection Bauermann et al.
Most cases of Hobi-like virus infection to date course subclinically or with mild disease and may, therefore, undergo undiagnosed. As a consequence, it is difficult to determine the economic impact of the disease. In addition, in regions where BVDV species and Hobi-virus cocirculate, the determination whether the economical losses are due to one virus or a "synergistic" effect of both is difficult to determine.
Identification of Hobi-like viruses may be overlooked at field conditions due clinical presentation resembling BVDV infection. In addition, biological products containing FBS should be carefully screened avoiding further dissemination of the agent. The spread of Hobi-like viruses into naive regions might have profound effects on cattle production, and may also affect the status of bovine pestivirus free that some regions achieved following immense efforts.
In Summer-Autumn , a novel virus associated with fever and drop in milk production was detected in cattle in northwestern Germany. Metagenomic analysis performed in blood samples from sick cattle revealed a new Orthobunyavirus Hoffmann et al. The agent was then temptatively named Schmallenberg virus SBV , a reference to the county of its first detection Tarlinton et al.
Following SBV detection in Germany, the emerging virus was detected causing diarrhea, abortion in cattle and fetal malformations in lambs in The Netherlands Doceul et al. Subsequently, the virus was detected in blood, bovine and sheep fetuses in several European countries, including Belgium, France, United Kingdom, Italy, Spain, etc. Antibodies to SBV were also detected in alpacas, bisons, deer, red deer and mouflons in Europe, without association with clinical disease Anonymous b.
At this point, the origin of SBV remains unclear. The virus may have come with insects from Africa or, alternatively, SBV might have been circulating unnoticed or latently in a reservoir host in Europe Tarlinton et al. Genomic analysis has led to the allocation of SBV in the Orthobunyavirus genus of the family Bunyaviridae. Bunyaviruses are large, enveloped viruses containing a single-stranded, negative sense, segmented RNA genome consisting of three segments large - L, medium - M and small - S Elliott The family comprises five genera: Hantavirus , Nairovirus , Orthobunyavirus , Phlebovirus and Tospovirus , and harbors important animal and human viruses, such as, akabane virus AkV and hantaviruses.
Sequence analysis of the three SBV genomic segments revealed similarity with Shamonda virus S segment: However, sequencing and phylogenetic analysis of several orthobunyaviruses indicates that SBV is more closely related to Sathuperi than to Shamonda virus, suggesting that the novel virus may be, in fact, an ancestor of Shamonda virus Goller et al. In any case, the definitive origin of this emerging virus is still uncertain and, as such, continues a matter of debate. Epidemiological studies demonstrated that SBV is transmitted by arthropod vectors, as most members of four genera of Bunyaviridae.
The SBV spreading in Europe is compatible with an arthropod vector and may reflect specific mosquito behavior revised by Doceul et al. Direct transmission between animals is very unlikely, yet the virus may spread directly across the placenta OIE The seroprevalence of SBV in European herds is variable but, in general, high antibody titers have been detected. Retrospective serological studies to in domestic ruminant sera identified seroprevalence ranging from 1.
In general, clinical signs associated with SBV infection are more severe in cows than in sheep and goats. Infected cows present fever, diarrhea, malaise, loss of appetite and drop in milk production Hoffmann et al. Infected animals develop short-lived viremia until days which is enough to produce fetal infection in pregnant females Hoffmann et al.
Pregnant sheep, goats and cows may present high incidence of abortions and congenital malformations revised by Doceul et al. The main malformations in the newborn are arthrogryposis, hydranencephaly, ataxia, torticollis, kyphosis, lordosis, scoliosis porencephaly, brain deformities and marked damage to the spinal cord Anonymous b. If the pathogenesis of SBV infection in pregnant ruminants is similar that of AkV, fetal malformations would vary depending of the stage of gestation in which the infection occurs Tarlinton et al.
Immunohistochemistry of the brain identifies SBV antigens in neurons of the grey matter and in the grey matter of the spinal cord Varela et al. In general, the pattern of lesions caused by SBV in domestic ruminants is similar to other orthobunyaviruses Herder et al. Serology to detect neutralizing antibodies can be performed by virus neutralization test VNT in serum samples from cattle and thoracic fluid samples from aborted or stillborn lambs and calves. SBV prevention and control include measures to reduce virus transmission and the development of vaccines.
Protection of susceptible animals from biting midges may also help in reducing exposure or infection Doceul et al. SBV is a new emerging virus producing important disease in cows, sheep and goats, and is currently a matter of important concern to veterinarians and animal health authorities in Europe. In this sense, sanitary measures and vaccination in development are important to avoid SBV spread and its introduction in other countries and continents. The viral particle is composed by a non-enveloped capsid, about 33 nm in diameter, which covers a single-stranded positive sense RNA genome of 7.
The whole genome is coupled to a poly-A tail Vasickova et al. The authors also reportedly found antibodies to HEV in 15 conventional herds in the Midwestern Meng et al. Even though HEV infections in human beings were not common at that time in the U. Nowadays, virtually all swine-producing countries have already reported the circulation of swine HEV. Although swine infection is spread worldwide, the cases of human HEV induced hepatitis are far more common in developing countries, indicating that poor levels of sanitation and inadequate disposal of swine manure may have an association with the epidemiology of human infection Meng Four main genotypes are identified, two of them circulate among pigs and humans, thus many authors recognize HEV as an emerging zoonotic virus Meng The disease caused by HEV in humans have some similarities with that caused by the Hepatitis A virus HAV , including the fecal-oral route of transmission and the absence of chronification.
Gross pathological lesions are absent both in naturally and experimentally infected animals. Microscopic lesions including mild to moderate multifocal periportal lymphoplasmacytic hepatitis are often reported in the liver of infected pigs, without clinical signs Meng et al. After infection, pigs become viremic and shed the virus on theirs feces from 8 days for up to 12 weeks. The immunity raised by the infection is long lasting and a prior infection with swine HEV prevents the onset of viremia and fecal shedding of the virus is also diminished in immune animals Meng et al.
Four genotypes were reported for HEV, named , based on the analysis of the complete genome sequence or partial genomic regions including a nt region in ORF1 and a nt region in ORF2 Mirazo et al. The genotype classification has a relationship with the host species infected and the geographical distribution of the virus Mirazo et al.
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Viruses from all 4 genotypes were found causing disease in humans, whereas only genotypes 3 and 4 are found in pigs. HEV genotypes were further subdivided into subtypes, however, the current separation into some of the subtypes specially within genotype 3 seems to be controversial Oliveira-Filho et al. Genotype 1 is mainly found in Asia and Africa, during HEV epidemics in humans; genotype 2 was firstly reported in Mexico and was further reported as an endemic virus in parts of Africa.
As mentioned before, those genotypes are restricted to humans Mirazo et al. Genotype 3 is worldwide distributed and has been causing infection in both humans and swines Oliveira-Filho et al. This genotype is often associated to epidemics of HEV liver disease in humans in South America and is also found on swine in this same region Oliveira-Filho et al. Moreover, genotype 3 HEV strains were also found in many other animal reservoirs including wild boar, rabbits, rats, deer and mongoose Vasickova et al.
Similarly, genotype 4 HEV was detected in humans and pigs, as well in wild boars Ishida et al. Genotype 4 is particularly important causing sporadic cases of hepatitis in humans in Asia, and in recently reported cases of human liver disease in France Okamoto Torovirus is a genus of viruses within the family Coronaviridae , subfamily Torovirinae that primarily infect vertebrates and include Berne virus of horses and Breda virus of cattle. They cause gastroenteritis in mammals, including humans but rarely. Influenza is caused by RNA viruses of the family Orthomyxoviridae and affects birds and mammals.
Wild aquatic birds are the natural hosts for a large variety of influenza A viruses. Occasionally viruses are transmitted from this reservoir to other species and may then cause devastating outbreaks in domestic poultry or give rise to human influenza pandemics. Fenner's Veterinary Virology, Fourth Edition. Bluetongue virus BTV , a member of Orbivirus genus within the Reoviridae family causes serious disease in livestock sheep, goat, cattle. It is non-enveloped, double-stranded RNA virus. The genome is segmented.
Circoviruses are small single-stranded DNA viruses. There are to genera: Herpesviruses are ubiquitous pathogens infecting animals and humans. African swine fever virus ASFV is a large double-stranded DNA virus which replicates in the cytoplasm of infected cells and is the only member of the Asfarviridae family. The virus causes a lethal haemorraghic disease in domestic pigs.
Some strains can cause death of animals within as little as a week after infection. In other species, the virus causes no obvious disease. ASFV is endemic to sub-Saharan Africa and exists in the wild through a cycle of infection between ticks and wild pigs, bushpigs and warthogs. Retroviruses are established pathogens of veterinary importance. They are generally a cause of cancer or immune deficiency.
Many flavivirus species can replicate in both mammalian and insect cells.