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Serum protein electrophoresis (SPE) is widely used to evaluate protein changes associated with several pathologies, aiming to assist clinical diagnosis. This study determines, for the first time, SPE profile changes in West Nile virus-naturally infected horses. Sixty horses with different clinical and infection status (encephalitis, asymptomatic infection, and immunologically naïve) were included. Total protein concentrations were determined via an automated biuret method and SPE was performed using a cellulose acetate membrane-based automated system. Statistical analysis revealed significantly higher total protein between both infected horse groups (encephalitis, asymptomatic) and naïve controls. Horses with encephalitis had higher globulin and α2-globulin levels than the other two groups (asymptomatic, naïve), along with lower albumin percentage and albumin-to-globulin ratio. Furthermore, γ-globulin levels were significantly higher in asymptomatically infected compared to control horses. These findings highlight the diagnostic value of SPE profile determination, assisting the clinicians, and providing the grounds for further research., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper, (Copyright © 2024 Elsevier Inc. All rights reserved.)

Of individuals who develop West Nile neuroinvasive disease (WNND), ~10% will die and >40% will develop long-term complications. Current treatment recommendations solely focus on supportive care; therefore, we urgently need to identify novel and effective therapeutic options. We observed a correlation between substance P (SP), a key player in neuroinflammation, and its receptor Neurokinin-1 (NK1R). Our study in a wild-type BL6 mouse model found that SP is upregulated in the brain during infection, which correlated with neuroinvasion and damage to the blood–brain barrier. Blocking the SP/NK1R interaction beginning at disease onset modestly improved survival and prolonged time to death in a small pilot study. Although SP is significantly increased in the brain of untreated WNND mice when compared to mock-infected animals, levels of WNV are unchanged, indicating that SP likely does not play a role in viral replication but may mediate the immune response to infection. Additional studies are necessary to define if SP plays a mechanistic role or if it represents other mechanistic pathways. [ABSTRACT FROM AUTHOR]

Of individuals who develop West Nile neuroinvasive disease (WNND), ~10% will die and >40% will develop long-term complications. Current treatment recommendations solely focus on supportive care; therefore, we urgently need to identify novel and effective therapeutic options. We observed a correlation between substance P (SP), a key player in neuroinflammation, and its receptor Neurokinin-1 (NK1R). Our study in a wild-type BL6 mouse model found that SP is upregulated in the brain during infection, which correlated with neuroinvasion and damage to the blood–brain barrier. Blocking the SP/NK1R interaction beginning at disease onset modestly improved survival and prolonged time to death in a small pilot study. Although SP is significantly increased in the brain of untreated WNND mice when compared to mock-infected animals, levels of WNV are unchanged, indicating that SP likely does not play a role in viral replication but may mediate the immune response to infection. Additional studies are necessary to define if SP plays a mechanistic role or if it represents other mechanistic pathways.

Background: Minimal data exist describing the epidemiology, management, and long‐term graft outcomes after West Nile viral disease in kidney transplant recipients (KTRs). Methods: Single‐center observational cohort study of patients who received a kidney transplant between 1/1/1994 and 12/31/2018 and developed WNV at any time point after transplantation. Results: During the 24‐year study period, 11 patients had documented WNV infection. Seven patients were recipients of a kidney transplant alone, and four had a simultaneous kidney and pancreas transplant. The mean age at the time of transplant was 44.7 ± 17.1 years, and the mean age at the time of WNV infection was 48 ± 17.2 years. All patients received lymphocyte depleting induction at transplant (alemtuzumab (n = 2), OKT3 (n = 1), or anti‐thymocyte globulin (n = 8)). The mean time from transplant to WNV infection was 3.4 ± 5.4 years, and none was suspected of having a donor‐derived infection. Three patients were treated for rejection in the 6 months before infection. The most common presenting symptom was altered mental status (n = 7), followed by a combination of fever and headache (n = 4). All patients had detectable serum WNV IgM antibodies at the time of diagnosis. All patients had a reduction in their immunosuppression and received supportive care; only two patients were treated with intravenous immunoglobulins. Nine patients recovered with no residual deficit; however, two suffered permanent neurologic damage. The mean estimated glomerular filtration rate drop at 1 year after the infection was 8.4 ± 13 mL/min/1.73 m2. Three patients suffered acute rejection within 1 year after the infection episode, likely attributable to aggressive immunosuppressive reduction. The mean follow‐up after the infection was 5.1 ± 4.3 years. At last follow‐up, two patients lost their kidney allograft, and five patients died. None of the graft losses or deaths occurred within a year of the WNV or were directly attributable to WNV. Conclusion: The majority of patients with WNV infection after KTR recovered fully with supportive care and immunosuppressive adjustment without residual neurologic sequelae. Additionally, WNV infection was associated with relatively small reductions in eGFR at 1 year. [ABSTRACT FROM AUTHOR]

While the central nervous system (CNS) was once thought to be excluded from surveillance by immune cells, a concept known as “immune privilege,” it is now clear that immune responses do occur in the CNS—giving rise to the field of neuroimmunology. These CNS immune responses can be driven by endogenous (glial) and/or exogenous (peripheral leukocyte) sources and can serve either productive or pathological roles. Recent evidence from mouse models supports the notion that infiltration of peripheral monocytes/macrophages limits progression of Alzheimer's disease pathology and militates against West Nile virus encephalitis. In addition, infiltrating T lymphocytes may help spare neuronal loss in models of amyotrophic lateral sclerosis. On the other hand, CNS leukocyte penetration drives experimental autoimmune encephalomyelitis (a mouse model for the human demyelinating disease multiple sclerosis) and may also be pathological in both Parkinson's disease and human immunodeficiency virus encephalitis. A critical understanding of the cellular and molecular mechanisms responsible for trafficking of immune cells from the periphery into the diseased CNS will be key to target these cells for therapeutic intervention in neurodegenerative diseases, thereby allowing neuroregenerative processes to ensue.

IntroductionWild birds and especially migratory species can become long-distance vectors for a wide range of microorganisms. The objective of the current paper is to summarize available literature on pathogens causing human disease that have been associated with wild bird species.MethodsA systematic literature search was performed to identify specific pathogens known to be associated with wild and migratory birds. The evidence for direct transmission of an avian borne pathogen to a human was assessed. Transmission to humans was classified as direct if there is published evidence for such transmission from the avian species to a person or indirect if the transmission requires a vector other than the avian species.ResultsSeveral wild and migratory birds serve as reservoirs and/or mechanical vectors (simply carrying a pathogen or dispersing infected arthropod vectors) for numerous infectious agents. An association with transmission from birds to humans was identified for 10 pathogens. Wild birds including migratory species may play a significant role in the epidemiology of influenza A virus, arboviruses such as West Nile virus and enteric bacterial pathogens. Nevertheless only one case of direct transmission from wild birds to humans was found.ConclusionThe available evidence suggests wild birds play a limited role in human infectious diseases. Direct transmission of an infectious agent from wild birds to humans is rarely identified. Potential factors and mechanisms involved in the transmission of infectious agents from birds to humans need further elucidation.

The economic burden of West Nile virus (WNV) infection is not known for Canada. We sought to describe the direct and indirect costs of WNV infection in the province of Quebec, Canada, up to 2 years after onset of signs and symptoms. We conducted a retrospective cohort study that included WNV cases reported during 2012 and 2013. For 90 persons infected with WNV, persons with encephalitis accounted for the largest proportion of total cost: a median cost of $21,332 per patient compared with $8,124 for West Nile meningitis (p = 0.0004) and $192 for West Nile fever (p<0.0001). When results were extrapolated to all reported WNV patients, the estimated total cost for 124 symptomatic cases was ≈$1.7 million for 2012 and that for 31 symptomatic cases was ≈$430,000 for 2013. Our study provides information for the government to make informed decisions regarding public health policies and infectious diseases prevention and control programs. [ABSTRACT FROM AUTHOR]

Over the past two decades, West Nile virus has become the most common arbovirus in North America, leading to several outbreaks and infecting thousands of people. Mosquitos help transmit the virus in the majority of cases, but transmission occurs via blood transfusions, organ transplantation, and possibly pregnancy and breastfeeding. While most infected patients experience mild to no symptoms, thousands of West Nile virus-associated neuroinvasive cases have been reported in the United States, with over 700 cases occurring in children from 2003 to 2016. Neuroinvasive disease presents as meningitis, encephalitis, or acute flaccid paralysis, and carries a high likelihood of poor outcome, including severe neurological disability or death. To date, no pharmacologic treatment has proven effective. Therapeutic clinical trials have not been successfully completed due to the sporadic nature of viral outbreaks and resultant poor study enrollment. Although older age and chronic disease are risk factors for neuroinvasive West Nile virus disease in adults, the specific factors that influence the risk in pediatric populations have not been fully elucidated. This review summarizes the most recent literature regarding West Nile virus-associated neuroinvasive disease, especially as it pertains to the pediatric population. Moreover, the review describes the epidemiology, clinical, laboratory, and radiographic findings, and outlines the various therapies that have been trialed and potential future research directions. [ABSTRACT FROM AUTHOR]

The West Nile virus is endemic in multiple European countries and responsible for several epidemics throughout the European region. Its evolution into local or even widespread epidemics is driven by multiple factors from genetic diversification of the virus to environmental conditions. The year of 2018 was characterized by an extraordinary increase in human and animal cases in the Central-Eastern European region, including Hungary. In a collaborative effort, we summarized and analyzed the genetic and serologic data of WNV infections from multiple Hungarian public health institutions, universities, and private organizations. We compared human and veterinary serologic data, along with NS5 and NS3 gene sequence data through 2018. Wild birds were excellent indicator species for WNV circulation in each year. Our efforts resulted in documenting the presence of multiple phylogenetic subclades with Balkans and Western-European progenitor sequences of WNV circulating among human and animal populations in Hungary prior to and during the 2018 epidemic. Supported by our sequence and phylogenetic data, the epidemic of 2018 was not caused by recently introduced WNV strains. Unfortunately, Hungary has no country-wide integrated surveillance system which would enable the analysis of related conditions and provide a comprehensive epidemiological picture. The One Health approach, involving multiple institutions and experts, should be implemented in order to fully understand ecological background factors driving the evolution of future epidemics.

Study objective: to perform assessment of the social and economic burden (analysis of the cost of disease) of five natural focal transmitted infectious diseases in theRussian Federationon the whole and in certain regions: ixodic tick-borne borreliosis, Siberian tick-borne typhus,Astrakhanrickettsial fever, Crimean hemorrhagic fever, andWest Nileencephalitis. Materials and methods. Direct and indirect costs caused with the studied diseases and the number of lost Disability Adjusted Life Years (DALY) are calculated in the probability model. Results. The total value of social and economic losses associated with vector-borne infectious diseases comprised 909 million rubles in prices of 2011; most of the value is represented with ixodid tick-borne borreliosis. Totally, these diseases cause the loss of 16,599 DALY.

The article presents data obtained during the observation of 18 children who had suffered fromWest Nileencephalitis. It is shown that WNE in theLower Volgaregion is characterized by extremely low morbidity in children. Unlike adults, the main clinical form of WNE in childhood is acute fever without damage to the central nervous system. The authors highlighted the leading clinical and laboratory syndromes: prolonged fever, neutrophilic leukocytosis, high frequency of secondary purulent bacterial complications.

Results of retrospective epidemiologic analysis of population morbidity in different regions of the Russian Federation and epidemic situation of West Nile fever in the territory of Russia are presented. Analysis was based on the reports of Rospotrebnadzor Administrations in the subjects of the Russian Federation and general publications of research institutes which carried out investigations of West Nile fever. Epidemic manifestations of this infection are identified in the Astrakhan, Volgograd, Rostov and Ulyanovsk regions. Circulation of West Nile virus is registered in 22 territories of Russia. The average seroprevalence of West Nile virus antibodies in population of different regions varies (1% in the West Siberia, 3% in the Rostov region and 10% in the Astrakhan, Volgograd regions and the Republic of Adygeya). The prognosis of epidemic development in near future demonstrated that spread of West Nile fever to the North territories of Russia would continue. The outbreaks of infection are possible in the territories where epidemic manifestations have not been noticed previously but virus circulation is identified in nature. The necessity of monitoring of West Nile virus in all territories of Russia is proved.

We reported an acute encephalitis syndrome outbreak in Alappuzha district in Kerala, India during the year 2011. The etiology was confirmed to be West Nile virus lineage 1. Many encephalitis patients from this outbreak exhibited neurological sequelae post recovery. This study was aimed to assess the clinical outcomes of West Nile encephalitis confirmed case-patients after 1 year of acute illness. Forty West Nile virus confirmed encephalitis patients were selected from the 2011 outbreak was included in this study. Out of 40 cases, only 30 survived after 12 months. Among these 30 recovered case-patients, 27 (90%) consented for clinical follow-up and 23 (73.67%) of them consented for assessment of cognitive impairment and deposition of blood sample for antibody testing. The most common symptom observed in these patients was fatigue (25.93%). Other symptoms included dizziness (7.4%), decreased sense of hearing (7.4%) and decreased sense of smell (7.4%). Reduced power in limbs was found in 33.33% of the cases. Most of the patients (23.1%) were dependent on others for normal daily living activities. The patients also had probable risk of poor cognition (29.41%) and dementia (57.14%). None of the patients were positive for WNV specific IgM at 12 months post onset of disease. The study concluded that the long-term sequelae were noticed in WNV positive patients. Prevention effort should be focused on the elderly (≥60 years old) people who have a higher risk of severe sequelae. The state health authorities should create awareness among people in order to prevent the transmission of disease. J. Med. Virol. 88:1856-1861, 2016. © 2016 Wiley Periodicals, Inc. [ABSTRACT FROM AUTHOR]

An outbreak of encephalitis occurred in New York City in late August 1999, the first caused by West Nile virus in North America. Histopathologic and immunopathologic examinations performed on human autopsy materials helped guide subsequent laboratory and epidemiologic investigations that led to identification of the etiologic agent.

West Nile virus (WNV), a mosquito-borne flavivirus, has increasingly become a concern in both America and Europe due to its complex and unpredictable lifecycle. Transfusion-associated transmission of the WNV has been well documented during the last few years. This study aimed to detect the presence of WNV in: (i) cerebrospinal fluid (CSF) specimens derived from aseptic meningitis cases in Greece and (ii) Greek blood donations. A total of 115 CSF specimens from patients suffering from aseptic meningitis and 9590 blood samples were collected from seven Greek hospitals during the periods June to October 2006 and 2007 and tested for investigational purposes. Both blood and CSF samples were tested for the presence of WNV RNA by using the PROCLEIX WNV assay. None of 115 CSF and 9590 blood donor samples was found positive according to our testing algorithms. Despite the presence of WNV in Balkan countries, WNV has not reached significant levels in Greece. [ABSTRACT FROM AUTHOR]

Abstract: Background: Computational methods are needed to design multivalent vaccines against flaviviruses (FVs) such as the West Nile virus or the dengue virus (DENV). Objective: We aimed to use physicochemical property (PCP) consensus sequences of FV strains to delineate conserved motifs, areas of maximum variability, and specific loci that correlate with arthropod vector, serotype, and disease severity. Methods: PCP consensus sequences for 27 species were prepared from 928 annotated sequences catalogued in Flavitrack. Alignments of these correlated well with the known structures of the NS3 protease domain and envelope (E) proteins. The PCPMer suite was used to identify motifs common to all FVs. Areas of PCP variability that correlated with phenotype were plotted on the structures. Results: Despite considerable diversity at the amino acid level, PCPs for both proteins were well conserved throughout the FVs. A series of insertions in E separated tick- from mosquito-borne viruses and all arthropod-borne viruses from isolates with no known vector or directly from insects. Comparison of a PCP consensus sequence of E derived from 600 DENV strains (DENV600) with individual ones for DENV1–DENV4 showed that most major serotype-specific variation occurs near these insertions. The DENV600 differed from one prepared from eight hemorrhagic or fatal strains from four DENV serotypes at only three positions, two of which overlap known escape mutant sites. Conclusions: Comparing consensus sequences showed that substantial changes occur in only a few areas of the E protein. PCP consensus sequences can contribute to the design of multivalent vaccines. [Copyright &y& Elsevier]

The West Nile virus is endemic in multiple European countries and responsible for several epidemics throughout the European region. Its evolution into local or even widespread epidemics is driven by multiple factors from genetic diversification of the virus to environmental conditions. The year of 2018 was characterized by an extraordinary increase in human and animal cases in the Central-Eastern European region, including Hungary. In a collaborative effort, we summarized and analyzed the genetic and serologic data of WNV infections from multiple Hungarian public health institutions, universities, and private organizations. We compared human and veterinary serologic data, along with NS5 and NS3 gene sequence data through 2018. Wild birds were excellent indicator species for WNV circulation in each year. Our efforts resulted in documenting the presence of multiple phylogenetic subclades with Balkans and Western-European progenitor sequences of WNV circulating among human and animal populations in Hungary prior to and during the 2018 epidemic. Supported by our sequence and phylogenetic data, the epidemic of 2018 was not caused by recently introduced WNV strains. Unfortunately, Hungary has no country-wide integrated surveillance system which would enable the analysis of related conditions and provide a comprehensive epidemiological picture. The One Health approach, involving multiple institutions and experts, should be implemented in order to fully understand ecological background factors driving the evolution of future epidemics. [ABSTRACT FROM AUTHOR]

West Nile encephalitis (WNE) presents clinically as aseptic meningitis, meningoencephalitis, encephalitis, or acute flaccid paralysis. Non-specific laboratory findings, e.g., leukopenia and thrombocytopenia, accompany WNE. Lymphopenia is marked and prolonged with WNE. Three patients with WNE were found to have elevated serum ferritin levels. Severity seemed to be directly related to serum ferritin levels. Although preliminary, the results suggested that serum ferritin levels ≥ 500 ng/mL (normal range 5–187 ng/mL) occur late with WNE, and not in a control group of patients with viral meningitis or encephalitis. [ABSTRACT FROM AUTHOR]