Enteric Viral Infections Research Articles

Study of Histopathological changes associated with FelinePan Leukopenia Virus infection in naturally infected cats

Feline Pan Leukopenia Virus (FPV) was the more serious enteric viral infection of cats at different periods of life. Also had different generalized effects on many vital organs. The current study, aimed to investigate the essential pathological lesions which caused by the virus infection. The study which carried out on 37 infected cats at age range from 3 – 36 months, these cats were checked previously at rapid test and PCR techniques .
 The autopsy samples were removed from infected animals and study the histopathological changes, including bowel, heart, spleen, tongue, kidney and lung, 10 pieces of each.The results had a significant effect on the animal's life . The histopathological findings were appeared at the level of severe acute infection ,thus lastly caused death. Furthermore, the results revealed that the virus can cause different inflammatory changes at different vital organs .
 Key Words . Feline parvovirus, Enteritis, histopathology .

Inverse Relationship Between Polio Incidence in the US and Colorectal Cancer.

Polio is predominantly an enteric viral infection that was progressively eradicated in the United States after the introduction of polio vaccine in the early 1950s. U.S. colorectal cancer rates have dropped steadily for individuals born between 1890 and 1950, but have been increasing for every generation born since 1950. Moreover, the lowest worldwide age adjusted rates of colorectal cancer in 2012 were in sub-Saharan Africa, Gambia and Mozambique, where polio has not been eradicated. In the current study, poliomyelitis incidence in US states before the introduction of polio vaccine was analyzed. Reported cases of poliomyelitis per 100,000 population by state 1932-1951 were from Centers for Disease Control. Colorectal cancer deaths per 100,000 in men (2005-2009) by US State are from the American Cancer Society. US state overweight and obesity data are from the Centers for Disease Control and Prevention (CDC). Smoking data are from the CDC. By US state, colorectal cancer incidence per 100,000 in men for 2005-2009 was inversely correlated with reported cases of poliomyelitis per 100,000 for 1932-1951 (r=-0.311, p=0.032). Colorectal cancer deaths per 100,000 in men in 2005-2009 were also inversely correlated with reported cases of poliomyelitis per 100,000 by state for 1932-1951 (r=-0.493, p<0.001). The relationship between colorectal cancer deaths and polio incidence was significant (β=-0.196, p=0.028) and independent of the effects of smoking (β=0.289, p=0.012) and overweight (β=0.547, p<0.001). The relationship in females with colorectal cancer was identical. Polio virus infection of cells of the colon may induce some degree of resistance to the development of colon cancer decades later. The effect of polio virus infection seems to be especially potent in reducing the rate of death from colon cancer.

Type III Interferon Restriction by Porcine Epidemic Diarrhea Virus and the Role of Viral Protein nsp1 in IRF1 Signaling.

Type III interferons (IFNs) play a vital role in maintaining the antiviral state of the mucosal epithelial surface in the gut, and in turn, enteric viruses may have evolved to evade the type III IFN responses during infection. To study the possible immune evasion of the type III IFN response by porcine epidemic diarrhea virus (PEDV), a line of porcine intestinal epithelial cells was developed as a cell model for PEDV replication. IFN-λ1 and IFN-λ3 inhibited PEDV replication, indicating the anti-PEDV activity of type III IFNs. Of the 21 PEDV proteins, nsp1, nsp3, nsp5, nsp8, nsp14, nsp15, nsp16, open reading frame 3 (ORF3), E, M, and N were found to suppress type III IFN activities, and IRF1 (interferon regulatory factor 1) signaling mediated the suppression. PEDV specifically inhibited IRF1 nuclear translocation. The peroxisome is the innate antiviral signaling platform for the activation of IRF1-mediated IFN-λ production, and the numbers of peroxisomes were found to be decreased in PEDV-infected cells. PEDV nsp1 blocked the nuclear translocation of IRF1 and reduced the number of peroxisomes to suppress IRF1-mediated type III IFNs. Mutational studies showed that the conserved residues of nsp1 were crucial for IRF1-mediated IFN-λ suppression. Our study for the first time provides evidence that the porcine enteric virus PEDV downregulates and evades IRF1-mediated type III IFN responses by reducing the number of peroxisomes.IMPORTANCE Porcine epidemic diarrhea virus (PEDV) is a highly contagious enteric coronavirus that emerged in swine in the United States and has caused severe economic losses. PEDV targets intestinal epithelial cells in the gut, and intestinal epithelial cells selectively induce and respond to the production of type III interferons (IFNs). However, little is known about the modulation of the type III IFN response by PEDV in intestinal epithelial cells. In this study, we established a porcine intestinal epithelial cell model for PEDV replication. We found that PEDV inhibited IRF1-mediated type III IFN production by decreasing the number of peroxisomes in porcine intestinal epithelial cells. We also demonstrated that the conserved residues in the PEDV nsp1 protein were crucial for IFN suppression. This study for the first time shows PEDV evasion of the type III IFN response in intestinal epithelial cells, and it provides valuable information on host cell-virus interactions not only for PEDV but also for other enteric viral infections in swine.

Developing the Molecular Genetic Component of Microbiological Monitoring of Nosocomial Acute Enteric Viral Infections

Developing the Molecular Genetic Component of Microbiological Monitoring of Nosocomial Acute Enteric Viral Infections

Estimation of health risks caused by exposure to enteroviruses from agricultural application of wastewater effluents

Agricultural reuse of wastewater is a common practice worldwide, especially in arid and semiarid area due to the freshwater scarcity. Wastewater irrigation in the Middle East, one of the most water-stressed regions in the world, could be a key factor for socio-economic development, but the microbial contamination of untreated or partially treated wastewater is a serious public health concern. Potential transmission of enteric viral infections through wastewater reuse in agricultural activities represents a true health risk for exposed individuals. Accordingly, it is important to assess the health risks associated with wastewater reuse. A quantitative microbial risk assessment (QMRA) with Monte-Carlo simulation was used to estimate the annual risk of enterovirus (EV) infection and disease burden for farmers and consumers of wastewater-irrigated lettuce in Iran, a semiarid country in the Middle East region. Risk analysis was performed based on the measured concentrations of EV in effluent of two activated sludge wastewater treatment plants (WWTP). Wastewater effluent sampling was carried out over a nine-month period, and the presence of total and fecal coliforms and EV was determined. Fecal coliform bacteria were found at a high level exceeded the guideline limit for wastewater reuse in agriculture. EVs were detected in 40% of samples with the highest frequency in summer with a mean of 12 and 16 pfu/ml for WWTP-A and B, respectively. Statistical analysis showed no correlation between the concentration of fecal coliforms and EV. The estimated infection risk for EVs was 8.8 × 10−1 and 8.2 × 10−1 per person per year (pppy) for farmers of WWTP-A and -B, respectively which was about 2 log higher than the tolerable infection risk of 2 × 10−3 pppy. The estimated risk for lettuce consumers exhibited a lower level of infection and disease burden but higher than the guideline limits. The median disease burden for consumption of lettuce irrigated with activated sludge effluents was about 10−3 Disability Adjusted Life Years (DALY) pppy which exceeded the WHO guideline threshold of 10−4 DALY pppy. The results of study indicated that the activated sludge effluents require an additional reduction of EVs to achieve the acceptable level of risk for agricultural reuse of wastewater.

Effect of Booster Vaccination with Inactivated Porcine Epidemic Diarrhea Virus on Neutralizing Antibody Response in Mammary Secretions.

Porcine epidemic diarrhea virus (PEDV) causes acute diarrhea, dehydration in pigs, and high mortality rates in piglets <3 weeks of age. Maternal immunity protects piglets, but information on vaccination before or after natural infection in endemically exposed sow herds is limited. Currently, the recovery goal in sow units infected with PEDV is to become fully naive again or use natural virus infection to develop immune gilts through a feedback program before introduction into the sow herd. Since neutralizing antibodies in the gut are critical for protection against enteric viral infections such as PEDV, we evaluated the effect of a conditionally licensed, adjuvanted inactivated PEDV vaccine on neutralizing antibody levels in milk and colostrum in both naive and previously naturally exposed sow herds. The results illustrate that intramuscular vaccination increased neutralizing antibody titers, and anti-PEDV IgA and IgG in milk and colostrum of sows that were previously infected. Thus, inactivated PEDV vaccines may provide increased protection to piglets nursing on previously infected sows against exposure to PEDV through increased delivery of lactogenic neutralizing antibodies to the enteric site of infection.

Interferon-Lambda: A Potent Regulator of Intestinal Viral Infections

Interferon-lambda (IFN-λ) is a recently described cytokine found to be of critical importance in innate immune regulation of intestinal viruses. Endogenous IFN-λ has potent antiviral effects and has been shown to control multiple intestinal viruses and may represent a factor that contributes to human variability in response to infection. Importantly, recombinant IFN-λ has therapeutic potential against enteric viral infections, many of which lack other effective treatments. In this mini-review, we describe recent advances regarding IFN-λ-mediated regulation of enteric viruses with important clinical relevance including rotavirus, reovirus, and norovirus. We also briefly discuss IFN-λ interactions with other cytokines important in the intestine, and how IFN-λ may play a role in regulation of intestinal viruses by the commensal microbiome. Finally, we indicate currently outstanding questions regarding IFN-λ control of enteric infections that remain to be explored to enhance our understanding of this important immune molecule.

Sex-Dependent Intestinal Replication of an Enteric Virus.

Coxsackievirus is an enteric virus that initiates infection in the gastrointestinal tract before disseminating to peripheral tissues to cause disease, but intestinal factors that influence viral replication are understudied. Furthermore, a sex bias for severe sequelae from coxsackievirus infections has been observed in humans. While mouse models mimicking human pathogenesis have been well characterized, many of these experiments use intraperitoneal injection of coxsackievirus to infect mice, bypassing the intestine. In light of recent studies identifying intestinal factors, such as the microbiota, that alter enteric viral replication, we sought to investigate coxsackievirus replication within the intestine. Here, we orally infected mice with coxsackievirus B3 (CVB3) and found that CVB3 replication in the intestine is sex dependent. CVB3 replicated efficiently in the intestine of male mice but not female mice. Additionally, we found that the type I interferon response and sex hormones can alter both viral replication and lethality. Overall, these data suggest that sex and the immune response play a vital role in CVB3 replication in the intestine and should be considered in light of the sex bias observed in human disease.IMPORTANCE Sex bias in severe sequelae from enteric viral infections has been observed. Since viruses have evolved to achieve optimal levels of fitness in their environmental niches, it is imperative to study viruses at the site of initial replication. Here, we used an oral inoculation system for CVB3, which follows the natural route of infection in the gastrointestinal tract. We found that sex can influence the replication of CVB3 in the intestine. Additionally, the type I interferon response and sex hormones alter both CVB3 intestinal replication and lethality. Overall this work highlights the fact that sex should be considered in investigations of enteric viral replication and pathogenesis.

Expression of Ifnlr1 on Intestinal Epithelial Cells Is Critical to the Antiviral Effects of Interferon Lambda against Norovirus and Reovirus.

Lambda interferon (IFN-λ) has potent antiviral effects against multiple enteric viral pathogens, including norovirus and rotavirus, in both preventing and curing infection. Because the intestine includes a diverse array of cell types, however, the cell(s) upon which IFN-λ acts to exert its antiviral effects is unclear. Here, we sought to identify IFN-λ-responsive cells by generation of mice with lineage-specific deletion of the receptor for IFN-λ, Ifnlr1 We found that expression of IFNLR1 on intestinal epithelial cells (IECs) in the small intestine and colon is required for enteric IFN-λ antiviral activity. IEC Ifnlr1 expression also determines the efficacy of IFN-λ in resolving persistent murine norovirus (MNoV) infection and regulates fecal shedding and viral titers in tissue. Thus, the expression of Ifnlr1 by IECs is necessary for the response to both endogenous and exogenous IFN-λ. We further demonstrate that IEC Ifnlr1 expression is required for the sterilizing innate immune effects of IFN-λ by extending these findings in Rag1-deficient mice. Finally, we assessed whether our findings pertained to multiple viral pathogens by infecting mice specifically lacking IEC Ifnlr1 expression with reovirus. These mice phenocopied Ifnlr1-null animals, exhibiting increased intestinal tissue titers and enhanced reovirus fecal shedding. Thus, IECs are the critical cell type responding to IFN-λ to control multiple enteric viruses. This is the first genetic evidence that supports an essential role for IECs in IFN-λ-mediated control of enteric viral infection, and these findings provide insight into the mechanism of IFN-λ-mediated antiviral activity.IMPORTANCE Human noroviruses (HNoVs) are the leading cause of epidemic gastroenteritis worldwide. Type III interferons (IFN-λ) control enteric viral infections in the gut and have been shown to cure mouse norovirus, a small-animal model for HNoVs. Using a genetic approach with conditional knockout mice, we identified IECs as the dominant IFN-λ-responsive cells in control of enteric virus infection in vivo Upon murine norovirus or reovirus infection, Ifnlr1 depletion in IECs largely recapitulated the phenotype seen in Ifnlr1-/- mice of higher intestinal tissue viral titers and increased viral shedding in the stool. Moreover, IFN-λ-mediated sterilizing immunity against murine norovirus requires the capacity of IECs to respond to IFN-λ. These findings clarify the mechanism of action of this cytokine and emphasize the therapeutic potential of IFN-λ for treating mucosal viral infections.

Use of dual priming oligonucleotide system-based multiplex RT-PCR combined with high performance liquid chromatography assay for simultaneous detection of five enteric viruses associated with acute enteritis

In this study, a specific and sensitive method for simultaneous detection of human astrovirus, human rotavirus, norovirus, sapovirus and enteric adenovirus associated with acute enteritis was developed, based on the specific dual priming oligonucleotide (DPO) system and the sensitive high-performance liquid chromatography (HPLC) analysis. The DPO system-based multiplex reverse transcription-polymerase chain reaction (RT-PCR) combined with HPLC assay was more sensitive than agarose gel electrophoresis analysis and real-time SYBR Green PCR assay, and showed a specificity of 100% and sensitivity of 96%–100%. The high sensitivity and specificity of the assay indicates its great potential to be a useful tool for the accurate diagnosis of enteric virus infections.

THE BURDEN AND FUTURE SCOPE FOR IMPORTANT VIRAL ENTERIC PATHOGENS IN AFRICA

BackgroundThe burden of viral enteric infections in Africa is enormous, although poorly described. Some, such as rotavirus, are well recognized, whereas others including norovirus or enteric adenovirus (EAd), show high...

Human Gut-On-A-Chip Supports Polarized Infection of Coxsackie B1 Virus In Vitro.

Analysis of enterovirus infection is difficult in animals because they express different virus receptors than humans, and static cell culture systems do not reproduce the physical complexity of the human intestinal epithelium. Here, using coxsackievirus B1 (CVB1) as a prototype enterovirus strain, we demonstrate that human enterovirus infection, replication and infectious virus production can be analyzed in vitro in a human Gut-on-a-Chip microfluidic device that supports culture of highly differentiated human villus intestinal epithelium under conditions of fluid flow and peristalsis-like motions. When CVB1 was introduced into the epithelium-lined intestinal lumen of the device, virions entered the epithelium, replicated inside the cells producing detectable cytopathic effects (CPEs), and both infectious virions and inflammatory cytokines were released in a polarized manner from the cell apex, as they could be detected in the effluent from the epithelial microchannel. When the virus was introduced via a basal route of infection (by inoculating virus into fluid flowing through a parallel lower ‘vascular’ channel separated from the epithelial channel by a porous membrane), significantly lower viral titers, decreased CPEs, and delayed caspase-3 activation were observed; however, cytokines continued to be secreted apically. The presence of continuous fluid flow through the epithelial lumen also resulted in production of a gradient of CPEs consistent with the flow direction. Thus, the human Gut-on-a-Chip may provide a suitable in vitro model for enteric virus infection and for investigating mechanisms of enterovirus pathogenesis.

A paradox of transcriptional and functional innate interferon responses of human intestinal enteroids to enteric virus infection.

The intestinal epithelium can limit enteric pathogens by producing antiviral cytokines, such as IFNs. Type I IFN (IFN-α/β) and type III IFN (IFN-λ) function at the epithelial level, and their respective efficacies depend on the specific pathogen and site of infection. However, the roles of type I and type III IFN in restricting human enteric viruses are poorly characterized as a result of the difficulties in cultivating these viruses in vitro and directly obtaining control and infected small intestinal human tissue. We infected nontransformed human intestinal enteroid cultures from multiple individuals with human rotavirus (HRV) and assessed the host epithelial response by using RNA-sequencing and functional assays. The dominant transcriptional pathway induced by HRV infection is a type III IFN-regulated response. Early after HRV infection, low levels of type III IFN protein activate IFN-stimulated genes. However, this endogenous response does not restrict HRV replication because replication-competent HRV antagonizes the type III IFN response at pre- and posttranscriptional levels. In contrast, exogenous IFN treatment restricts HRV replication, with type I IFN being more potent than type III IFN, suggesting that extraepithelial sources of type I IFN may be the critical IFN for limiting enteric virus replication in the human intestine.

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Case-control study of diarrheal disease etiology in individuals over 5years in southwest China.

BackgroundAcute diarrhea is one of the major public health problems worldwide. Most of studies on acute diarrhea have been made on infants aged below 5 years and few efforts have been made to identify the etiological agents of acute diarrhea in people over five, especially in China.Methods271 diarrhea cases and 149 healthy controls over 5 years were recruited from four participating hospitals between June 2014 and July 2015. Each stool specimen was collected to detect a series of enteric pathogens, involving five viruses (Rotavirus group A, RVA; Norovirus, NoV; Sapovirus, SaV; Astrovirus, As; and Adenovirus, Ad), seven bacteria (diarrheagenic Escherichia coli, DEC; non-typhoidal Salmonella, NTS; Shigella spp.; Vibrio cholera; Vibrio parahaemolyticus; Aeromonas spp.; and Plesiomonas spp.) and three protozoa (Cryptosporidium spp., Giardia lamblia, G. lamblia, and Blastocystis hominis, B. hominis). Standard microbiological and molecular methods were applied to detect these pathogens. Data was analyzed using Chi square, Fisher-exact tests and logistic regressions.ResultsThe prevalence of at least one enteric pathogen was detected in 29.2% (79/271) acute diarrhea cases and in 12.1% (18/149) in healthy controls (p < 0.0001). Enteric viral infections (14.4%) were the most common in patients suffering from acute diarrhea, followed by bacteria (13.7%) and intestinal protozoa (4.8%). DEC (12.5%) was the most common causative agent in diarrhea cases, followed by NoV GII (10.0%), RVA (7.4%) and B. hominis (4.8%). The prevalence of co-infection was statistically higher (p = 0.0059) in the case group (7.7%) than in the healthy control (1.3%). RVA–NoV GII (3.0%) was the most common co-infection in symptomatic cases.ConclusionsDEC was the most predominant pathogen in diarrhea cases, but it was largely overlooked because the lack of laboratory capacities. Because of the high prevalence of co-infections, it is recommended the urgent development of alternative laboratory methods to assess polymicrobial infections. Such methodological improvements will result in a better prevention and treatment strategies to control diarrhea illness in China.Electronic supplementary materialThe online version of this article (doi:10.1186/s13099-016-0141-1) contains supplementary material, which is available to authorized users.

Oral Administration of Astrovirus Capsid Protein Is Sufficient To Induce Acute Diarrhea In Vivo.

ABSTRACTThe disease mechanisms associated with the onset of astrovirus diarrhea are unknown. Unlike other enteric virus infections, astrovirus infection is not associated with an inflammatory response or cellular damage. In vitro studies in differentiated Caco-2 cells demonstrated that human astrovirus serotype 1 (HAstV-1) capsid protein alone disrupts the actin cytoskeleton and tight junction complex, leading to increased epithelial barrier permeability. In this study, we show that oral administration of purified recombinant turkey astrovirus 2 (TAstV-2) capsid protein results in acute diarrhea in a dose- and time-dependent manner in turkey poults. Similarly to that induced by infectious virus, TAstV-2 capsid-induced diarrhea was independent of inflammation or histological changes but was associated with increased intestinal barrier permeability, as well as redistribution of sodium hydrogen exchanger 3 (NHE3) from the membrane to the cytoplasm of the intestinal epithelium. Unlike other viral enterotoxins that have been identified, astrovirus capsid induces diarrhea after oral administration, reproducing the natural route of infection and demonstrating that ingestion of intact noninfectious capsid protein may be sufficient to provoke acute diarrhea. Based on these data, we hypothesize that the astrovirus capsid acts like an enterotoxin and induces intestinal epithelial barrier dysfunction.

Compromised Defenses: Exploitation of Epithelial Responses During Viral-Bacterial Co-Infection of the Respiratory Tract.

Respiratory infections are the greatest single contributor to the overall burden of disease worldwide [1]. Polymicrobial infections are becoming increasingly recognized in terms of both prevalence and their effect on disease severity, causing many common diseases such as oral infections, otitis media, chronic wound infections, and implanted medical device infections, as well as chronic pulmonary disease in cystic fibrosis patients [2,3]. There is a large body of literature demonstrating synergy between viral and bacterial infections at mucosal surfaces; for example, (i) the intestinal microbiota promotes enteric viral infection via direct interactions and modulation of the immune system [4]; (ii) sexually transmitted viruses exploit the altered environment, including altered pH, inflammatory, and oxidative settings, during bacterial vaginosis or aerobic vaginitis to increase infection of the vaginal and cervical epithelium [5]; and (iii) bacteria take advantage of the altered innate and adaptive immune responses of the respiratory tract during viral infection of the respiratory epithelium to increase infectivity and virulence [6]. Many studies have focused on the consequences of influenza infection on secondary bacterial infection in the respiratory tract, where altered lung physiology and immune status increases susceptibility to severe secondary bacterial infections with common commensal organisms of the upper respiratory tract, such as Streptococcus pneumoniae and Staphylococcus aureus [7]. Here, we focus on the role of the respiratory epithelium in defending against microbial pathogens as well as in facilitating synergistic pathogenic interactions (Fig 1). Fig 1 Model of increased susceptibility to secondary bacterial infection after primary viral infection of the respiratory epithelium. Role of the Respiratory Epithelium in Innate and Adaptive Immunity The respiratory epithelium is the primary site of host–pathogen encounter in the respiratory tract and the first line of defense against infection (extensively reviewed [8–10]). The epithelium employs a wide array of tools to inhibit colonization as well as dictate innate and adaptive immune responses to pathogens that overcome these initial barriers. First and foremost, the epithelium is a physical barrier to pathogen invasion, forming cell–cell junctions to exclude pathogens from the underlying tissues and actively restrict nutrient availability. Respiratory epithelial cells maintain an airway surface liquid into which they secrete mucins that form a mucus layer to trap and propel pathogens out of the respiratory tract via mucociliary beat. The epithelium also secretes many additional effectors in the airway surface liquid, including antimicrobial peptides and proteins, such as degradative enzymes, iron sequestration proteins, protease inhibitors, collectin surfactant proteins, chemokines, and various forms of palate-lung-nasal-clone protein (PLUNC). The airway epithelium also produces toxic reactive nitrogen species and reactive oxygen species. These direct antimicrobial effectors are upregulated in response to pathogen or pro-inflammatory signals. Airway epithelial cells also produce cytokines and chemokines in response to pathogens, via pattern recognition receptor (PRR) activation, or to pro-inflammatory signals to shape the innate and adaptive immune responses, leading to an influx of neutrophils and monocytes, differentiation of monocytes into dendritic cells and macrophages, influx and activation of Th cells, and differentiation of B cells. B cell differentiation leads to immunoglobulin (Ig) class switching, and epithelial cells transcytose polymeric IgM and IgA into the airway surface liquid. Despite this array of defense functions, synergistic interactions between viral and bacterial respiratory pathogens can arise when one pathogen is able to suppress the antimicrobial activities of the epithelium or when an epithelial response that is protective against one pathogen makes the airway more permissive for infection by the other pathogen.

Relationship between different enteric viral infections and the occurrence of diarrhea in broiler flocks in Jordan

The aim of this study is to determine if enteric viruses are the cause of diarrhea in broiler flocks in Jordan. Intestinal content samples were collected from 101 broiler flocks from several regions of Jordan to detect the presence of astrovirus, coronavirus, reovirus, and rotavirus, by using reverse transcriptase polymerase chain reaction (RT-PCR). Forty-six of these flocks were clinically healthy with no enteric disease, and the other 55 flocks were clinically suffering from diarrhea. The samples were collected between 5 and 16 d of age. The results show that 79% of total 101 flocks tested were infected with one or more of the above enteric viruses. Coronavirus was the most common virus, detected in 56.4% of these flocks, with astrovirus in 29.7% of the flocks, and rotavirus (9.9%) and reovirus (5.6%) being the least common. None of these flocks were found to be infected with all four viruses, but one of the flocks was found to be infected with astrovirus, coronavirus, and rotavirus simultaneously. Individual infection was noted with astrovirus, coronavirus and rotavirus but not with reovirus, whereas all flocks infected with reovirus were also infected with coronavirus. There was no statistical evidence to link these viruses as the main cause of diarrhea in the flocks tested. This is the first study in Jordan to detect all of these viruses and to correlate their presence with diarrhea in chicken flocks.

Characterization of a genetically heterogeneous porcine rotavirus C, and other viruses present in the fecal virome of a non-diarrheic Belgian piglet

Next-generation sequencing (NGS) technologies are becoming increasingly accessible, leading to an expanded interest in the composition of the porcine enteric virome. In the present study, the fecal virome of a non-diarrheic Belgian piglet was determined. Although the virome of only a single piglet was analyzed, some interesting data were obtained, including the second complete genome of a pig group C rotavirus (RVC). This Belgian strain was only distantly related to the only other completely characterized pig RVC strain, Cowden. Its relatedness to RVC strains from other host species was also analyzed and the porcine strain found in our study was only distantly related to RVCs detected in humans and cows. The gene encoding the outer capsid protein VP7 belonged to the rare porcine G3 genotype, which might be serologically distinct from most other pig RVC strains. A putative novel RVC VP6 genotype was identified as well. A group A rotavirus strain also present in this fecal sample contained the rare pig genotype combination G11P[27], but was only partially characterized. Typical pig RVA genotypes I5, A8, and T7 were found for the viral proteins VP6, NSP1, and NSP3, respectively. Interestingly, the fecal virome of the piglet also contained an astrovirus and an enterovirus, of which the complete genomes were characterized. Results of the current study indicate that many viruses may be present simultaneously in fecal samples of non-diarrheic piglets. In this study, these viruses could not be directly associated with any disease, but still they might have had a potential subclinical impact on pig growth performance. The fast evolution of NGS will be a powerful tool for future diagnostics in veterinary practice. Its application will certainly lead to better insights into the relevance of many (sub)clinical enteric viral infections, that may have remained unnoticed using traditional diagnostic techniques. This will stimulate the development of new and durable prophylactic measures to improve pig health and production.

Defensins Potentiate a Neutralizing Antibody Response to Enteric Viral Infection.

α-defensins are abundant antimicrobial peptides with broad, potent antibacterial, antifungal, and antiviral activities in vitro. Although their contribution to host defense against bacteria in vivo has been demonstrated, comparable studies of their antiviral activity in vivo are lacking. Using a mouse model deficient in activated α-defensins in the small intestine, we show that Paneth cell α-defensins protect mice from oral infection by a pathogenic virus, mouse adenovirus 1 (MAdV-1). Survival differences between mouse genotypes are lost upon parenteral MAdV-1 infection, strongly implicating a role for intestinal defenses in attenuating pathogenesis. Although differences in α-defensin expression impact the composition of the ileal commensal bacterial population, depletion studies using broad-spectrum antibiotics revealed no effect of the microbiota on α-defensin-dependent viral pathogenesis. Moreover, despite the sensitivity of MAdV-1 infection to α-defensin neutralization in cell culture, we observed no barrier effect due to Paneth cell α-defensin activation on the kinetics and magnitude of MAdV-1 dissemination to the brain. Rather, a protective neutralizing antibody response was delayed in the absence of α-defensins. This effect was specific to oral viral infection, because antibody responses to parenteral or mucosal ovalbumin exposure were not affected by α-defensin deficiency. Thus, α-defensins play an important role as adjuvants in antiviral immunity in vivo that is distinct from their direct antiviral activity observed in cell culture.