Mosquito pool surveillance is a cornerstone of arbovirus risk assessment, yet traditional metrics such as the minimum infection rate (MIR) can understate infection probability and, as conventionally reported, do not provide uncertainty quantification that properly accounts for pooling. We analyzed 7 yr (2018-2024) of mosquito pool surveillance data using pooled maximum likelihood estimation (MLE) with transformed Clopper-Pearson confidence intervals to estimate per-mosquito infection probabilities. The dataset comprised 4,930 pools (246,500 mosquitoes) collected across 80 surveillance sites and tested for 6 arbovirus assay targets covering eastern equine encephalitis, St. Louis encephalitis, West Nile, chikungunya, dengue, and Zika viruses. Viral circulation was sparse (5 positive pools, 0.10% overall positivity), but the pooled-likelihood framework still produced interpretable infection-probability estimates together with conservative upper confidence bounds in zero-positive and sparse-positive weeks. Peak infection probabilities ranged from 0.678 per 1,000 mosquitoes for West Nile virus in August 2022 to 2.667 per 1,000 for chikungunya and Zika virus detections in October 2018. In this low-positivity setting, MIR, pooled MLE, and the Firth/Burrows bias-reduced estimator were numerically close in the observed positive weeks, whereas the main practical gain came from interval estimates that made sampling uncertainty explicit. These results support moving from MIR-only summaries to a broader pooling-aware reporting framework in mosquito surveillance. Reporting both per-mosquito infection estimates and interval bounds places sparse detections and zero-positive weeks on a common operational scale and supports interpretation alongside other surveillance indicators.

Hand, foot, and mouth disease (HFMD) is a common viral illness that predominantly affects young children, with approximately 95% of cases occurring in individuals under the age of 5. While typically self-limiting, a subset of cases may present with more severe cardiopulmonary and neurological sequelae, such as myocarditis, pneumonia, meningitis, and encephalitis. Management is primarily supportive, as no standard antiviral therapy currently exists. However, previous case reports have suggested that acyclovir may offer therapeutic benefits. We present a case of a healthy 39-year-old female who experienced dramatic symptomatic improvement within 10 hours and complete resolution within 48 hours following off-label valacyclovir use. This case raises the possibility of valacyclovir use in adults with HFMD and highlights the need for further research to validate its role.

Japanese Encephalitis Virus (JEV) is a mosquito-borne zoonotic pathogen that triggers severe inflammatory responses upon infection. Previous research has demonstrated that the interaction between Ras-associated GTP-binding protein 4B (Rab4b) and the JEV E protein is essential for the virus's entry into early endosomes. However, the precise mechanism by which Rab4b contributes to JEV-induced inflammatory responses remains inadequately understood. In this study, we developed a Rab4b-knockout U251 cell model and found that Rab4b deficiency markedly inhibited viral replication and concurrently reduced levels of key inflammatory mediators, including IL-1β, IL-6, TNF-α, and IFN-β. Transcriptomic analysis further indicated that the loss of Rab4b disrupted the Toll-like receptor 3 (TLR3)-related gene network. Subsequent co-immunoprecipitation experiments confirmed an interaction between Rab4b and TLR3, and treatment with a TLR3 inhibitor recapitulated the anti-inflammatory phenotype observed in Rab4b-deficient cells, suggesting the involvement of Rab4b in TLR3-related signaling. In conclusion, these findings support an association between Rab4b and a TLR3-related inflammatory signaling axis during JEV infection, although the precise mechanistic relationship requires further investigation.

West Nile virus neuroinvasive disease (WNND) most commonly presents as meningitis, encephalitis, or acute flaccid paralysis, with variable neuroimaging findings. While MRI abnormalities classically involve deep gray matter and brainstem structures, hemorrhagic manifestations are rarely reported. We report a 77-year-old woman who presented with rapidly progressive altered mental status following a brief febrile prodrome. Cerebrospinal fluid studies demonstrated a lymphocytic pleocytosis consistent with aseptic meningitis. Brain MRI revealed an acute lacunar infarct and diffuse cerebral microhemorrhages initially concerning for cerebral amyloid angiopathy. During hospitalization, she developed livedo reticularis-like peripheral skin changes prompting evaluation for autoimmune or vasculitic etiologies. Extensive infectious and autoimmune testing was ultimately notable for positive serum and CSF West Nile virus serologies, confirming neuroinvasive WNV infection. Despite transient neurologic improvement, her clinical course deteriorated, and she died following transition to comfort-focused care. This case highlights diffuse cerebral microhemorrhages as a potential finding in WNND, although their attribution remains uncertain. These findings may reflect underlying neurovascular inflammatory injury related to WNV or may represent coincident pathology and can mimic other small-vessel or autoimmune pathologies, complicating early diagnostic evaluation. Recognition of this expanded radiographic and clinical spectrum may aid timely diagnosis of WNND in patients with atypical presentations.

In this report, we describe a 19-day-old female neonate who presented with recurrent apnea, poor feeding, and cyanosis. Brain diffusion-weighted MRI revealed hyperintense lesions in the genu of the corpus callosum and bilateral frontal white matter with corresponding low apparent diffusion coefficient values. Antibiotic therapy and supportive management were initiated, and the apnea resolved by hospital day 6. A follow-up brain MRI performed on day 49 demonstrated the complete resolution of the previously observed lesions. No neurological sequelae were observed up to 11 months of age. This case illustrates a rare presentation of neonatal-onset apnea associated with reversible lesions localized in the genu of the corpus callosum on MRI. Several differential diagnoses were considered, including mild encephalitis/encephalopathy with a reversible splenial lesion (MERS)-related conditions, viral encephalitis, postictal changes, and pre-Wallerian degeneration. When reversible corpus callosum lesions are observed in neonates, a variety of underlying pathophysiological processes should be considered in the differential diagnosis.

Sudden death due to rhombencephalitis is a rare and life-threatening inflammatory condition, infrequently reported in forensic literature. Rhombencephalitis and acute necrotizing encephalitis (ANE) are uncommon but severe inflammatory disorders of the central nervous system, often linked to viral infections. Both may present with seizures, altered sensorium, and rapid neurological deterioration leading to fatal outcomes. We describe the case of an 18-year-old previously healthy female who developed high-grade fever followed by seizures and progressive encephalopathy. Neuroimaging showed diffuse cerebral edema with bilateral thalamic hyperintensities, raising the possibility of ANE, complicated by intracranial circulatory arrest. Despite supportive measures, the patient succumbed within 24 hours. Histopathologic examination revealed lymphocytic infiltration of the brainstem, pontine microhemorrhages, and absent thalamic necrosis, favoring viral rhombencephalitis rather than necrotizing encephalitis. This case illustrates the clinicoradiological overlap between rhombencephalitis and ANE and highlights the diagnostic and medicolegal challenges in sudden deaths due to fulminant viral encephalitic syndromes.

Orthoflaviviruses are etiological agents of neurological diseases in equines. Horses are susceptible to equine Tick-borne encephalitis virus (TBEV), Usutu virus (USUV), and West Nile virus (WNV), although mostly WNV has been associated with clinical disease. The aim of the present study was to estimate the prevalence of TBEV, USUV and WNV in 289 healthy horses from nine provinces of Algeria. This study was conducted between March 2021 and December 2023. Sera that tested positive, doubtful, or negative close to the doubtful threshold in the Orthoflavivirus-ELISA were further tested by the virus neutralization test (VNT), using TBEV, USUV, and WNV strains. The prevalence of Orthoflaviviruses antibodies by ELISA was 23.18% (67/289) compared with 16.95% (49/289) and 0.69% (2/289) detected by WNV and USUV VNT, respectively. TBEV antibodies were not detected in any samples. WNV seroprevalence varied with age, breed, climatic zones and altitude of the horses' locations. This is the first screening of horse sera for TBEV in Algeria. This study indicates that WNV and USUV have circulated/are circulating in the horse population in three Algerian climatic zones, unlike TBEV, which does not seem to be present.

Rift Valley fever virus (RVFV) causes haemorrhagic fever, ophthalmitis, and in severe cases, encephalitis in humans. Despite the well-recognised neurotropism, the mechanisms of central nervous system (CNS) invasion remain poorly understood. We investigated RVFV ingress into the CNS and resulting neuropathogenesis following intranasal inoculation in ferrets (Mustela putorius furo) (n = 15). At 3 DPI, before RVFV dissemination to the CNS, mild multifocal suppurative rhinitis and multifocal interstitial pneumonia were detected in the nasal cavity and lungs respectively, supported by detection of viral antigen and genome. From 6 DPI, infected ferrets exhibited neurological signs; by 6 - 8 DPI, a mild-to-moderate non-suppurative meningoencephalitis and myelitis was observed, progressing rostrally to caudally, with ophthalmitis observed from 7 DPI and 100% mortality by 8 DPI. Mild-to-moderate hyperaemia of the meninges was identified macroscopically in all infected ferrets. An immune response to infection was unable to prevent neuropathogenesis and clinical disease. Although our results suggest that neuroinvasion occurs via the olfactory route through the nasal turbinates to cranial nerves, virus replication in the lungs and presence of viremia implies that haematogenous dissemination into the CNS as a secondary route is possible. This relevant experimental ferret model may further contribute to understanding the pathogenesis of human RVFV infection.