Virus Infection Research Articles

An overview of oral pediatric infectious diseases

Pediatric oral infectious diseases, caused by a range of viral, bacterial, and fungal pathogens, represent a significant challenge in clinical practice. These infections, often influenced by age, immune status, and hygiene practices, can lead to pain, functional impairments, and systemic complications. Common viral infections such as herpetic gingivostomatitis, varicella-zoster virus (VZV) manifestations, and hand-foot-and-mouth disease present with characteristic oral lesions, often accompanied by systemic symptoms. Bacterial infections, including dental caries, gingivitis, and odontogenic infections, are primarily linked to microbial colonization, dietary habits, and poor oral hygiene. Advanced cases, such as necrotizing periodontal diseases, can have severe implications if not managed promptly. Fungal infections, predominantly caused by Candida species, occur frequently in neonates and immunocompromised children, manifesting as oral thrush or angular cheilitis, and require targeted antifungal therapy. Prevention strategies, including the use of fluoride, dietary counseling, and regular dental check-ups, play a pivotal role in reducing the incidence of these infections. Management approaches vary based on the pathogen and clinical severity, ranging from supportive care and antifungal agents to antibiotic therapy and surgical interventions in severe cases. Collaborative care between dental practitioners and other healthcare providers is essential for effective outcomes. Infection control measures within dental settings and public health initiatives, such as vaccination and oral health education, are crucial in minimizing transmission and recurrence. Addressing pediatric oral infectious diseases requires a multifaceted approach, incorporating individualized patient care, preventive measures, and public health strategies to promote optimal oral and systemic health outcomes. Continued research and innovation are vital to improving diagnostic tools and therapeutic options for managing these infections in pediatric populations.

Long-term impact of congenital Zika virus infection on the rat hippocampus: Neuroinflammatory, glial alterations and sex-specific effects.

Congenital Zika Syndrome (CZS) is a condition that arises when a neonate presents with abnormalities resulting from Zika virus infection during gestation. While microcephaly is a prominent feature of the syndrome, other forms of brain damage are also observed, often accompanied by significant neurological complications. It is therefore essential to investigate the long-term effects of CZS, with special attention to sex differences, particularly concerning hippocampal function, given its vulnerability to viral infections. The aim of this study was to evaluate the long-term impacts on cognitive and memory functions, as well as neuroinflammatory and glial alterations in the hippocampus, in offspring of both sexes exposed to a model of congenital Zika virus infection. Pregnant rats were subcutaneously inoculated with ZIKV-BR at a dose of 1 × 10^7 plaque-forming units (PFU mL^-1) of ZIKV isolated in Brazil (ZIKV-BR) on gestational day 18 (G18). From postnatal day 70, the animals underwent behavioral tests. On postnatal day 80, the animals were euthanized, and hippocampal samples were collected for biochemical and histological analyses. In the open field test, females displayed more exploratory behavior and less grooming, while no significant differences in locomotion were observed between the sexes. Additionally, ZIKV-exposed females showed a reduction in grooming behavior compared to ZIKV-exposed males. In the memory test, males in the ZIKV group exhibited greater memory impairment, spending more time to locate the correct quadrant, while females showed relatively better performance. Neuroinflammatory markers, such as TNF-α, were significantly elevated in the hippocampus of ZIKV-exposed animals, regardless of sex. However, microglial and astrocytic responses, indicated by higher IBA1 and GFAP density, were only observed in male ZIKV rats. In conclusion, our findings suggest that congenital ZIKV exposure leads to sex-specific behavioral and neuroinflammatory alterations. While both males and females exhibited some behavioral changes, males were more significantly impacted in memory performance. Additionally, increased neuroinflammatory markers and glial activation were observed in the hippocampus of ZIKV-exposed animals, with a pronounced response in males. These results highlight the long-term impact of ZIKV infection on neurodevelopment, emphasizing the importance of considering sex differences in studies of congenital ZIKV syndrome.

Epidemiological characteristics of eleven common respiratory viral infections in children

BackgroundLower respiratory tract infections (LRTIs) are one of the leading causes of hospital admissions among children. In this study, we aimed to describe the epidemiological characteristics of viral pathogens associated with LRTIs in hospitalized children in Yan’an; this has yet to be reported in the literature and may guide public health interventions and resource allocation in this region.MethodsBetween June 2021 and May 2023, we conducted a retrospective analysis of the results of viral detection using oral pharyngeal swabs from 4565 children with LRTIs in the Inpatient Department of Yan’an University Affiliated Hospital. Eleven respiratory viruses, including influenza A virus (Flu A), influenza A H1N1 virus (H1N1), seasonal influenza A H3N2 virus (H3N2), influenza B virus (Flu B), parainfluenza virus (HPIV), adenovirus (HADV), bocavirus (HBoV), rhinovirus (HRV), metapneumovirus (HNPV), coronavirus (HCoV), and respiratory syncytial virus (HRSV), were confirmed by applying a multiplex real-time polymerase chain reaction (PCR) kit for respiratory viruses. We evaluated the epidemiological features of infections caused by respiratory pathogens, including aging, gender and the seasonal variations of different pathogens, and explored the high-risk factors associated with virus-caused pneumonia.ResultsAt least one virus was detected in all 4565 cases; the positivity rate was 27.95%. We also detected a total of 1,276 cases with mixed infections (with two or more viruses). Of the positive cases, 59.3% were male and 40.7% were female (x2 = 0.41, P = 0.68). The highest positivity rates for respiratory pathogens were observed for HRSV, HRV, and HADV, at 5.98%, 5.67%, and 4.38%, respectively. We also observed variations in the number and positivity rates of respiratory pathogen infections by season, age and gender. HPIV (x2 = 12.05, P < 0.05) and HADV (x2 = 11.73, P < 0.05) were more common in children under three years-of-age. Notably, with the exception of the 1 to < 3 years age group, males consistently demonstrated elevated infection rates across other age groups.ConclusionsOur analysis revealed that respiratory pathogen infections varied by gender, season, and age in the enrolled population of children.

Structural basis of different neutralization capabilities of monoclonal antibodies against H7N9 virus.

Neutralizing antibodies (nAbs) are important for the treatment of emerging viral diseases and for effective vaccine development. In this study, we generated and evaluated three nAbs (1H9, 2D7, and C4H4) against H7N9 influenza viruses and found that they differ in their ability to inhibit viral attachment, membrane fusion, and egress. We resolved the cryo-electron microscopy (cryo-EM) structures of H7N9 hemagglutinin (HA) alone and in complex with the nAb antigen-binding fragments (Fabs) and identified the HA head-located epitope for each nAb, thereby revealing the molecular basis and key residues that determine the differences in these nAbs in neutralizing H7N9 viruses. Moreover, we found that the humanized nAb CC4H4 provided complete protection in mice against death caused by a lethal H7N9 virus infection, even when nAb was given 3 days after the mice were infected. These findings provide new insights into the neutralizing mechanism and structural basis for the rational design of H7N9 virus vaccines and therapeutics.IMPORTANCEH7N9 viruses have caused severe infections in both birds and humans since their emergence in early 2013 in China. Their persistent presence and variation in avian populations pose a significant threat to both poultry and humans. There are no treatments for human infections. In this study, we thoroughly investigated the neutralization mechanisms, structural basis, and therapeutic effects of three nAbs (1H9, 2D7, and C4H4) against H7N9 viruses. We revealed the molecular determinants underlying the varied performances of the three nAbs in neutralizing H7N9 viruses and protecting H7N9-infected mice. These insights provide a solid foundation for the rational design of vaccines and therapeutics against H7N9 viruses.

The complexity of the interpretation of ELISA and RT-PCR results in the diagnosis of a reticuloendotheliosis virus infection: an extended case study

ABSTRACT Reticuloendotheliosis virus (REV) is a species of the genus Gammaretrovirus that can cause neoplasia, immunosuppression, and runting-stunting syndrome. To show the clinical relevance of REV is complicated, and requires the demonstration of the virus, REV antibodies, the presence of typical gross and microscopic lesions, and the exclusion of other oncogenic agents in the case of the presence of tumours. Under field conditions, the first tests to be used might be a commercially available REV antibody ELISA or an RT-PCR to detect the REV genome. In this short paper, we present the experiences with two commercially available ELISAs and RT-PCR that we have gained from a REV outbreak on a large multi-age layer farm and many follow-up tests on samples from control farms with and without a known history of REV and fowlpox virus (FPV). In the field, some of the FPV field strains contain large inserts of the REV genome that might interfere with REV testing. The results of the ELISAs on sera from REV- and FPV- unsuspected flocks suggested that the cut-offs of both ELISAs were somewhat low resulting in a lower specificity. However, cut-offs of 2000 and 3050 for the IDEXX and BioChek ELISAs, respectively, gave an agreement of 100%, suggesting that these cut-offs might be advisable to use. The use of the combination of RT-PCR for REV and PCR for FPV proved to be very useful in separating REV infections from FPV infections. The results of our extended field study can help to interpret REV testing results.

Persistent Epstein-Barr Virus Infection of Epithelial Cells Leads to APOBEC3C Expression and Induces Mitochondrial DNA Mutations.

Upon infection with the virus, cells increase the expression of cytidine deaminase APOBEC3 family genes. This leads to the accumulation of C-to-T mutations in the replicating viral genome and suppresses viral propagation. In contrast, herpesviruses, including Epstein-Barr virus (EBV), express genes that counteract APOBEC3 during lytic infection. However, because viral resistance factors are not expressed during EBV latent infection, it is unknown how APOBEC3 functions during latent infection. We observed that in gastric epithelial cells persistently infected with EBV, the expression of APOBEC3 family genes increased, C-to-T mutations in the D-loop genome of mitochondrial DNA (mtDNA) increased, and mtDNA copy number decreased. By introducing and expressing individual APOBEC3 family genes, APOBEC3C was particularly expressed in the cytoplasm, increasing C-to-T mutations in mtDNA and decreasing mtDNA copy number. Furthermore, we confirmed that APOBEC3C co-localized with mitochondria in EBV-infected cells. Expression of the EBV latent gene LMP2A increased APOBEC3C expression. Conversely, APOBEC3C expression was reduced in LMP2A-deficient EBV-infected cells compared to wild-type EBV-infected cells. These results indicate that persistent infection of EBV in gastric epithelial cells reduces the number of mitochondria through mtDNA mutations induced by APOBEC3C expression.

Detecting Monkeypox Virus by Immunohistochemistry.

Mpox (formerly known as monkeypox), a zoonotic disease caused by Monkeypox virus (MPXV), has become an international outbreak since May 2022. Mpox often presents with a mild systemic illness and a characteristic vesiculopustular skin eruption. In addition to molecular testing, histopathology of cutaneous lesions usually showsdistinctive findings, such as epidermal necrosis, balloon degeneration, papillary dermal edema, and focal dermal necrosis, which have proven helpful in the diagnosis of mpox. Viral cytopathic changes with areas of multinucleation, smudging of the nuclei, and intracytoplasmic inclusions have also been described. Although useful, these features are relatively nonspecific. The use of a monoclonal antibody for immunohistochemical (IHC) staining of MPXV may be a useful tool in confirming mpox infection. Three cases of PCR-confirmed mpox were biopsied and subjected to IHC staining with a monoclonal MPXV-specific antibody targeting viral envelope protein A29. As controls, cell lines transduced to express other MPXV viral antigens and samples of cutaneous viral infections involving Molluscum contagiosum, Herpes simplex, Herpes zoster, or Cytomegalovirus were also subjected to IHC staining with this antibody. All three mpox patient biopsies performed on lesional skin subjected to MPXV IHC staining reliably detected viral infection in lesional skin with a diffuse cytoplasmic and focally nuclear staining pattern. No staining was seen in transduced cell lines expressing off-target MPXV viral antigens and in lesional skin of other common viral infections listed above. The monoclonal MPXV-specific antibody may be used as an adjunct tool to confirm mpox infection.

DYRK4 upregulates antiviral innate immunity by promoting IRF3 activation.

Viral infection activates the transcription factors IRF3 and NF-κB, which induce type I interferon (IFN) and antiviral innate immune responses. Here, we identify dual-specific tyrosine phosphorylation-regulated kinase 4 (DYRK4) as an important regulator of virus-triggered IFN-β induction and antiviral innate immunity. Overexpression of DYRK4 enhances virus-triggered activation of IRF3 and type I IFN induction, whereas knockdown or knockout of DYRK4 impairs virus-induced activation of IRF3 and NF-κB. Moreover, Dyrk4-knockout mice are more susceptible to viral infection. The underlying mechanism involves DYRK4 acting as a scaffold protein to recruit TRIM71 and LUBAC to IRF3, increasing IRF3 linear ubiquitination, maintaining IRF3 stability and activation during viral infection, and promoting the IRF3-mediated antiviral response. Our findings provide new insights into the molecular mechanisms underlying viral infection-triggered IRF3 stabilization and activation.

Functional Involvement of Signal Transducers and Activators of Transcription in the Pathogenesis of Influenza A Virus

Signal transducers and activators of transcription (STATs) function both as signal transducers and transcription regulators. STAT proteins are involved in the signaling pathways of cytokines and growth factors; thus, they participate in various life activities and play especially critical roles in antiviral immunity. Convincing evidence suggests that STATs can establish innate immune status through multiple mechanisms, efficiently eliminating pathogens. STAT1 and STAT2 can activate the antiviral status by regulating the interferon (IFN) signal. In turn, suppressor of cytokine signaling-1 (SOCS1) and SOCS3 can modulate the activation of STATs and suppress the excessive antiviral immune response. STAT3 not only regulates the IFN signal, but also transduces Interleukin-6 (IL-6) to stimulate the host antiviral response. The function of STAT4 and STAT5 is related to CD4+ T helper (Th) cells, and the specific mechanism of STAT5 remains to be studied. STAT6 mainly exerts antiviral effects by mediating IL-4 and IL-13 signaling. Here, we reviewed the recent findings regarding the critical roles of STATs in the interactions between the host and viral infection, especially influenza A virus (IAV) infection. We also discuss the molecular mechanisms underlying their functions in antiviral responses.

Impact of SARS-CoV-2 on the male reproductive tract: insights from semen analysis and cryopreservation.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the virus behind the COVID-19 pandemic, affects multiple organs, including the male reproductive system. While viral infections can harm male fertility through cytokine storms, the effects of SARS-CoV-2 on fertility are still unclear. Thus, this study aimed to examine the persistence of viral RNA and inflammatory responses in semen following SARS-CoV-2 infection and the safety of conventional freezing and vitrification techniques. Semen samples from 20 patients were collected 3months post-SARS-CoV-2 infection. Samples underwent freezing and vitrification. Molecular and cellular analysis separated seminal plasma and pellets. Flow cytometry characterized immune cells. Viral RNA was extracted from plasma and sperm, followed by RT-qPCR. Cytometric Bead Array measured cytokine levels. Angiotensin-converting enzyme 2 (ACE2) and transmembrane serine protease 2 (TMPRSS2) receptors were detected in both plasma and sperm fractions. Five patients exhibited viral RNA-dependent RNA polymerase, indicating potential persistence. Elevated inflammatory cytokines in plasma implied persistent inflammation affecting sperm vitality. Immune cells associated with viral clearance were identified in semen, correlating with receptor expression and cytokines. Both conventional freezing and vitrification were found safe procedures for preserving male fertility. Our study highlights the impact of SARS-CoV-2 on male reproductive health, emphasizing the persistence of viral entry receptors, potential viral RNA presence, the inflammatory environment, and the involvement of immune populations in the male reproductive tract post-infection. Importantly, we confirm the safety of conventional freezing and vitrification techniques for preserving male fertility in assisted reproductive technology programs amidst the COVID-19 pandemic.

Guillain-Barré syndrome.

Guillain-Barré syndrome (GBS) is a rare immune-mediated polyradiculoneuropathy. Patients typically develop rapidly progressive weakness and sensory deficits that can result in complete paralysis requiring mechanical ventilation. GBS is usually a monophasic disease in which an aberrant immune response to an infection or other trigger damages the peripheral nerves. For example, in patients with preceding Campylobacter jejuni infection, molecular mimicry causes a cross-reactive antibody response to nerve gangliosides. Diagnosis is based on clinical features, supported by cerebrospinal fluid analysis and nerve conduction studies. Effective treatments include plasma exchange and intravenous immunoglobulins. However, ~20% of patients who received treatment are unable to walk after 6 months and ~5% die as a consequence of GBS. Important knowledge gaps in GBS include its pathogenesis, especially after viral infections. In addition, there is a lack of specific biomarkers to improve thediagnosis, monitor thedisease activity, and predict the clinical course and outcome of GBS. Major challenges for the future include finding more effective and personalized treatments, which are affordable in low-income and middle-income countries, and preparation for outbreaks of infections as potential triggers for GBS.

Testing perioperative meloxicam analgesia to enhance welfare while preserving model validity in an inflammation-induced seizure model

Despite the international effort to improve laboratory animal welfare through the 3R principles (Reduce, Refine, Replace), many scientists still fail to implement and report their assessment of pain and well-being, likely due to concerns regarding the potential effects of analgesics on experimental outcomes. This study aimed to determine whether refining our viral encephalitis model with perioperative analgesia could enhance well-being and recovery after intracerebral virus infection without impacting disease outcomes. We routinely use the Theiler’s Murine Encephalomyelitis Virus (TMEV) model to study virus-induced epilepsy. Given the crucial role of immune cell activation in acute seizure development, we evaluated the effects of the non-steroidal anti-inflammatory drug (NSAID) meloxicam on inflammation, neurodegeneration, and neuronal cell proliferation at 7 days post-infection (dpi). Overall, the impact of virus infection on well-being was less severe than anticipated, and meloxicam treatment did not affect well-being or nest building behavior in TMEV-infected mice. Furthermore, meloxicam treatment did not influence key experimental readouts such as seizure burden, central inflammatory response, neurodegeneration, or neuronal proliferation within the hippocampus. Notably, animals experiencing seizures displayed heightened inflammatory responses and neurodegeneration, which were not influenced by meloxicam treatment. In summary, perioperative analgesia did not compromise key outcome measures such as seizure frequency, inflammation, and neurodegeneration or -regeneration in the TMEV model. However, it also did not add any significant benefits to well-being in the first week after intracranial injections.

Impact of daily prompt to vaccinate inpatients awaiting rehabilitation against SARS-CoV-2 and influenza.

A daily prompt to offer vaccination to inpatients awaiting transfer to rehabilitation resulted in increased SARS-CoV-2 (OR 5.64, 95% CI 3.3-10.15; P < 0.001) and influenza (OR 3.80, 95% CI 2.45-6.06; P < 0.001) vaccination. Compared to baseline, this intervention was associated with reduced incidence of viral respiratory infection during subsequent admission to rehabilitation.

The alphavirus determinants of intercellular long extension formation.

The alphavirus chikungunya virus (CHIKV) is a serious human pathogen that can cause large-scale epidemics characterized by fever and joint pain and often resulting in chronic arthritis. Infection by alphaviruses including CHIKV and the closely related Semliki Forest virus (SFV) can induce the formation of filopodia-like intercellular long extensions (ILEs). ILEs emanate from an infected cell, stably attach to a neighboring cell, and mediate cell-to-cell viral transmission that is resistant to neutralizing antibodies. However, our mechanistic understanding of ILE formation is limited, and the potential contribution of ILEs to CHIKV virulence or human CHIKV infection is unknown. Here, we used well-characterized virus mutants and monoclonal antibodies with known epitopes to dissect the virus requirements for ILE formation. Our results showed that both the viral E2 and E1 envelope proteins were required for ILE formation, while viral proteins 6K and transframe, and cytoplasmic nucleocapsid formation were dispensable. A subset of CHIKV monoclonal antibodies reduced ILE formation by masking specific regions particularly on the E2 A domain. Studies of the viral proteins from different CHIKV strains showed that ILE formation is conserved across the four major CHIKV lineages. Sera from convalescent human CHIKV patients inhibited ILE formation in cell culture, providing the first evidence for ILE inhibitory antibody production during human CHIKV infections.IMPORTANCEChikungunya virus (CHIKV) infections can cause severe fever and long-lasting joint pain in humans. CHIKV is disseminated by mosquitoes and is now found world-wide, including in the Americas, Asia, and Africa. In cultured cells, CHIKV can induce the formation of long intercellular extensions that can transmit virus to another cell. However, our understanding of the formation of extensions and their importance in human CHIKV infection is limited. We here identified viral protein requirements for extension formation. We demonstrated that specific monoclonal antibodies against the virus envelope proteins or sera from human CHIKV patients can inhibit extension formation. Our data highlight the importance of evaluation of extension formation in the context of human CHIKV infection.

Persistence of hepatitis E vaccine-induced antibody response across different dosage schedules and baseline serostatus

Hepatitis E virus (HEV) infection is a major cause of acute viral hepatitis worldwide. The efficacy and safety of the HEV239 vaccine have been validated, with protection lasting at least 10 years. This study extended the phase 3 trial of HEV239 (NCT01014845), presenting data on the durability of the anti-HEV IgG response elicited by one or two doses in the participants with different baseline serostatus. Over half of baseline seronegative individuals retained detectable antibodies at month 91 after two doses, with geometric mean concentration levels above the detection limit at month 67 (no available data for month 91). Seropositive individuals exhibited more prolonged and higher anti-HEV IgG response. After a single dose, individuals with pre-existing immunity achieved high and sustained antibody levels for over 103 months, comparable to the two-dose regimen. Both single-dose and two-dose HEV239 regimens demonstrated notable immunogenicity and persistence, potentially offering substantial protective benefits.

Establishing an immune correlate of protection for Nipah virus in nonhuman primates

The limited but recurrent outbreaks of the zoonotic Nipah virus (NiV) infection in humans, its high fatality rate, and the potential virus transmission from human to human make NiV a concerning threat with pandemic potential. There are no licensed vaccines to prevent infection and disease. A recombinant Hendra virus soluble G glycoprotein vaccine (HeV-sG-V) candidate was recently tested in a Phase I clinical trial. Because NiV outbreaks are sporadic, and with a few cases, licensing will likely require an alternate regulatory licensing pathway. Therefore, determining a reliable vaccine correlate of protection (CoP) will be critical. We assessed the immune responses elicited by HeV-sG-V in African Green monkeys and its relationship with protection from a NiV challenge. Data revealed values of specific binding and neutralizing antibody titers that predicted survival and allowed us to establish a mechanistic CoP for NiV Bangladesh and Malaysia strains.

Kidney function impairment among adult people living with HIV on antiretroviral therapy in South-West, Nigeria

BackgroundHuman immunodeficiency virus (HIV) infection and use of antiretroviral therapy (ART) pose a significant risk of causing kidney function impairment in people living with HIV (PLHIV) and could contribute to their morbidity and mortality. Clinicians and healthcare providers ought to encourage routine screening for kidney function to optimize therapy in this disease population. The aim of this study is to assess the prevalence and predictors of kidney function impairment among HIV patients on ART. We conducted a retrospective cohort analysis on electronic data collected among HIV patients ≥ 18 years who received ART between 2006 and 2023. Patients’ demographic data, clinical data and ART received were retrieved. Each patient’s estimated glomerular filtration rate (eGFR) assessed accordingly. Descriptive statistics and logistic regression analysis were done using SPSS 29.02 software.ResultsOut of 1026 HIV patients on ART data analyzed in this study, 66.9% were females and the prevalence of kidney function impairment (eGFR < 60 mL/min/1.73 m2) was 42.5%. Factors associated with kidney function impairment identified were tenofovir disoproxil fumarate (TDF) based regimen [aOR = 225.3 (CI: 89.5–567.2), p < 0.001], female gender [aOR = 6.67, (CI: 4.48–9.92), p < 0.001], WHO clinical stage [aOR = 2.64 (CI: 1.47–4.73), p < 0.001], and CD4 count [aOR = 2.51 (CI: 1.56–4.05), p < 0.001].ConclusionThere is a high prevalence of kidney function impairment among PLHIV on ART and could be associated with female gender, CD4 cell count, WHO clinical stage and the use of TDF-based regimen. We recommend early screening for kidney function before commencing ART and monitoring for timely intervention to reduce the risk for further damage to the kidneys.

Surveillance of Schmallenberg virus in cattle populations in Northeastern Brazil.

The objective of this study was to conduct a serological investigation of Schmallenberg virus (SBV) infection in cattle raised in the State of Alagoas. A total of 460 serum samples from the Agricultural Defense Agency of Alagoas (ADEAL) serum bank were analyzed. These samples were collected from unvaccinated cattle on 100 properties across 99 municipalities in Alagoas, representing the three mesoregions: Agreste, Leste, and Sertão. Serological diagnosis was performed using commercial indirect Enzyme-Linked Immunosorbent Assay (ELISA) kit. The results showed that 0.87% (4 out of 460) of the samples yielded questionable results in the indirect ELISA (with calculated percentages > 50.00% and ≤ 60.00%). Upon further testing with competitive ELISA, only one sample tested positive. These findings underscore the need to strengthen regional surveillance and control strategies for emerging pathogens. Additionally, further studies, including viral isolation from both ruminants and vectors, are crucial to confirm the circulation of this pathogen. Such comprehensive investigations are essential for improving our understanding of SBV dynamics and for developing effective control measures.

Isolation of porcine epidemic diarrhea virus strain CHCQ-2023 from Chongqing Province and analysis of S gene recombination

BackgroundIn recent years, the prevalence and incidence of porcine epidemic diarrhea virus (PEDV) infection have been on the rise. The occurrence of multiviral infections and recombination mutations has led to accelerated viral evolution and reduced vaccine efficacy. In the present study, a PEDV strain was isolated from a pig farm (Chongqing Province, China) with an outbreak of porcine diarrhea, and its S gene was found to be recombinant.ResultsThe optimal trypsin concentration for blind passage of PEDV in Vero cells was determined to be 7.5 µg/mL. Following two blind passages of the virus in Vero cells, the virus was unable to adapt to the cells. Therefore, PEDV was blindly passaged in IPEC-J2 cells using the optimal concentration of trypsin (5 µg/mL). Next, a series of characterization experiments were performed. Recombination analyses of the isolates using software revealed that the S gene of strain CHCQ-2023 was derived from the primary parent strain PEDV-1 C and secondary parent strain SQ2014, with recombination occurring at a 3152 bp breakpoint. Furthermore, a specific B-cell antigenic epitope was predicted on the S2 subunit of the S protein.ConclusionA PEDV strain was isolated and characterized, and its S gene was characterized. The findings provide a bioinformatic basis for the study of PEDV strain variation due to genetic recombination.

The effect of spatial variation on linkage to care and treatment rates among patients with hepatitis C: A Canadian population-based study

Introduction: Despite significant global efforts towards eliminating hepatitis C virus (HCV) infection, multiple challenges remain in achieving this goal. In this study, we assessed the impact of geographical variation on HCV diagnosis and treatment rates in Alberta, Canada. Methods: Adults aged ≥20 years with a positive HCV antibody were identified from the provincial administrative sources from the fiscal years 2012 through 2017. To assess the differences across Alberta's rural-urban continuum, high-resolution spatial analyses using global and local spatial autocorrelation were applied to the HCV age- and sex-standardized prevalence rate at the sub-local geographic area level. We compared and tested differences in HCV RNA tests, HCV RNA positivity rates, and HCV treatment status across the different areas. Results: Between 2012 and 2017, we identified 18,768 patients who had tested positive for HCV Ab. Within this cohort, only 63.1% had HCV RNA repetitive. The HCV RNA positivity rate was 42.1%, and 65.3% had received HCV treatment after testing as HCV RNA positive. HCV Ab positive case counts exhibited a spatial distribution consistent with that of the population at risk: 67.5% in metro, 11.1% in urban, 19.7% in rural, and 1.8% in remote areas. The metropolitan area of Edmonton's age-and sex-standardized prevalence of 8.2 (95% CI 8.0–8.4) per 1,000 persons was higher than Calgary's standardized prevalence of 5.0 (95% CI 5.1–5.4) per 1,000 persons ( p &lt; 0.001). HCV RNA and HCV treatment rates demonstrated significant spatial variation. Conclusions: HCV prevalence, diagnosis, and treatment exhibit significant spatial variation across rural-urban Alberta. Implementation of geographically oriented screening and treatment interventions would result in a time- and cost-efficient HCV elimination strategy.