Journal of NeuroVirology最新文献

Background: Postherpetic neuralgia (PHN) represents the most prevalent and distressing complication of shingles. The aim of this study was to explore the diagnostic significance of miR-34c-5p in PHN patients and to assess its correlation with rehabilitation effect.

Methods: This study enrolled 154 PHN patients and 108 healthy participants as research subjects. RT-qPCR was used to detect serum miR-34c-5p levels in the participants. ROC curve was employed to estimate the diagnostic significance of miR-34c-5p in PHN patients. Logistic regression analysis was performed to analyze the risk factors related to the occurrence of PHN. VAS, TEX-Q and HADS scales were filled in by questionnaires to analyze the rehabilitation effect of PHN patients after treatment. Spearman correlation analysis was applied to evaluate the relationship of miR-34c-5p levels with rehabilitation effect in treated PHN patients.

Results: miR-34c-5p levels were notably elevated in PHN patients compared to healthy participants. miR-34c-5 had a high sensitivity (79.2%) and specificity (84.3%) to distinguish between healthy individuals and PHN patients. Logistic regression analysis indicated that miR-34c-5p emerged as an independent risk factor for the development of PHN. miR-34c-5p levels, VAS, TEX-Q, HADS-A and HADS-D scores were reduced in prednisone-treated PHN patients compared to the basic treatment group. In addition, Spearman correlation suggested that miR-34c-5p levels were positively correlated with VAS, TEX-Q, HADS-A and HADS-D scores.

Conclusion: miR-34c-5p exhibited the ability to diagnose PHN and may be a biomarker for diagnosis of this disease. Moreover, reduced miR-34c-5p expression in PHN patients correlate with enhanced outcomes in rehabilitation.

Misuse of opioids is a major comorbidity in people with HIV (PWH). Neurological abnormalities and opioid addiction seen in PWH involve the interplay among signaling pathways. However, the impact of HIV proteins on morphine dependence is understudied. We aimed to understand the modulation of the opioid dependence genes and signaling pathways in the striatum (Str) and prefrontal cortex (PFC) of PWH. HIV-1 transgenic (HIV-1Tg) rats and F344 control animals were given 2 and 4 pellets of morphine (75-mg/pellet)/placebo on Days 1 and 2, respectively, via subcutaneous implantation. On Day 5, at morphine tolerance the rats were sacrificed, Str and PFC were collected for RNA isolation and cDNA preparation. A PCR-array was used to examine the expression of the 65 opioid dependance genes. Varying numbers of genes were significantly upregulated in the Str and PFC of morphine treated rats. Fold change values were uploaded to QIAGEN Ingenuity Pathway Analysis, to study the signaling pathways associated with the treatment conditions. CREB signaling in neurons and Neuroinflammation signaling pathway were highly activated in the Str of both male and female HIV-1Tg rats given morphine. Gαq signaling and S100 family signaling were activated in female HIV-1Tg rats received morphine. Similarly, in the PFC, synthesis of IP3, CREB Signaling in neurons, Gαq signaling in males and CREB Signaling in neuron, and Gαq signaling in females were activated. Using bioinformatic analysis, we identified key signaling pathways and gender dependent changes in the opioid dependent gene expression and pathway enrichment of HIV-1Tg rats at morphine tolerance.

The development of a comprehensive classification for herpesvirus encephalitis remains an urgent task. Distinct clinic-radiological forms of herpesvirus cerebral lesions have been characterized, including findings from histopathological studies. Differences among these forms have been demonstrated concerning key clinical and paraclinical parameters. The presented classification identifies several distinct forms of herpesvirus encephalitis: temporal, brainstem, limbic, diencephalic encephalitis, rhombencephalitis, leukoencephalitis, ventriculoencephalitis, diffuse glial micronodular encephalitis, subcortical and cortical encephalitis, cerebellitis, neonatal encephalitis. Additionally, the concepts of combined, coexisting and multimodal lesions are introduced to describe complex forms of herpesvirus neuroinfections. The use of the term "specific spectrum of herpesvirus cerebral lesions" is supported. Both the phenomena of specificity and universality are considered. Fundamental differences between the forms of herpesvirus encephalitis are highlighted with respect to their prevalence within the population, etiological factors, clinical manifestations, typical complications, recovery completeness, mortality rates, immune status. The distinctive diagnostic and therapeutic approaches required for each form of herpesvirus encephalitis are emphasized. The integration of this classification into clinical practice has the potential to optimize medical care for patients with herpesvirus encephalitis, enabling not only etiologically-oriented but also form-specific approaches to treatment.

HIV-associated neurocognitive disorders (HAND) pose significant challenges, particularly in individuals with comorbid opioid use disorder (OUD). Fentanyl, a potent synthetic opioid, is a leading contributor to opioid-related fatalities, yet its effects in the context of HIV remain poorly understood. This study investigated the differential impacts of fentanyl and morphine on neuroinflammatory signaling, blood-brain barrier (BBB) integrity, and antiretroviral (ARV) brain accumulation in EcoHIV-infected mice. C57BL/6 mice were assigned to morphine, fentanyl, or saline treatment groups, with or without EcoHIV infection. Tight junction proteins claudin-5 and ZO-1 were measured in striatum and hippocampus via ELISA, while proinflammatory chemokines were analyzed by multiplex assay. In EcoHIV-infected mice, both opioids significantly increased CCL2, CCL4, CCL5, and CCL11 concentrations in the striatum, with fentanyl causing greater increases in CCL2 than morphine. Additionally, fentanyl, but not morphine, significantly decreased CCL3 concentrations in the striatum. Principal component analysis revealed distinct treatment-specific patterns within the striatum, underscoring opioid-specific differences. Tight junction protein expression data demonstrate opioid-specific, sex-specific, and region-specific effects on the key BBB proteins, ZO-1 and claudin-5. Both opioids also reduced ARV brain concentrations in infected mice, with region- and opioid-specific effects. Fentanyl decreased dolutegravir in the hippocampus, while morphine decreased abacavir in both regions. These findings demonstrate that fentanyl and morphine exposure in the context of HIV produce distinct impacts on neuroinflammatory response, BBB integrity, and ARV brain exposure. Understanding these opioid-specific effects is critical for improving clinical outcomes and treatment strategies for individuals with HIV and OUD.

Crimean-Congo hemorrhagic fever is a severe tick-borne viral infection with high mortality rates. While Crimean-Congo hemorrhagic fever primarily presents as a hemorrhagic fever, central nervous system involvement, including encephalitis, is rare. The virus, transmitted through tick bites or direct contact with infected animal blood or bodily fluids, can lead to multi-organ failure. Neurological manifestations of Crimean-Congo hemorrhagic fever remain poorly understood. We report a 40-year-old man from Hormozgan province, Iran, who presented with fever, hematemesis, abdominal pain, and neurological symptoms. Initial laboratory findings indicated thrombocytopenia and elevated liver enzymes. Despite treatment with ribavirin, the patient developed agitation, confusion, and a progressive decline in consciousness. Brain imaging suggested encephalitis, and cerebrospinal fluid analysis revealed mild pleocytosis with elevated protein levels. Crimean-Congo hemorrhagic fever was confirmed via polymerase chain reaction testing. The patient was treated with ribavirin, intravenous immunoglobulin, and high-dose methylprednisolone, gradually recovering neurological function. Crimean-Congo hemorrhagic fever with encephalitis is an uncommon but severe presentation, necessitating prompt diagnosis and intervention. This case highlights the potential role of corticosteroids and intravenous immunoglobulin in managing Crimean-Congo hemorrhagic fever-associated neurological manifestations. Further studies are needed to establish standardized treatment protocols for Crimean-Congo hemorrhagic fever-related encephalitis.

Facial palsy refers to facial muscle paralysis and is typically brought about by viral infections, such as herpes simplex virus type 1 (HSV-1), herpes zoster virus (VZV), and SARS-CoV-2. While significant progress has been achieved in viral facial palsy pathogenesis, mechanisms of viral infection-immunity synergy are yet to be revealed. The authors of this article made an attempt to fill this gap by critically summarizing how viral infection causes inflammation and damage to the facial nerve through an immune response mechanism in the facial palsy pathogenesis. We also summarize the current treatment modalities and their respective efficacies. The article set the conditions under which viral infections caused by HSV-1, VZV, SARS-CoV-2, HIV, and EBV lead to facial paralysis and how the viruses infect the facial nerve, initiate an immune response, and cause nerve death. The impact involved direct viral invasion of neurons, immune evasion and induction of neuroinflammation. The review also discusses the primary role of T cells, B cells and innate immune cells in inducing or relieving the condition. The study emphasizes the need to understand the synergic effect of viral infection and immuneresponse of facial palsy as the foundation of the creation of more potent therapeutic strategies. The paper provides a detailed overview of complex interaction of immuneresponse and viral infection of facial palsy with significant level of importance regarding future research and clinical application.

Background: JC polyomavirus (JCPyV) is a globally prevalent human polyomavirus that establishes lifelong latency, primarily in renal tissue. Despite its global importance, molecular epidemiological data on JCPyV still remain limited.

Objectives: This study aimed to investigate the prevalence, genotype distribution, and genetic variations of JCPyV in urine and plasma samples from people living with HIV (PLWH) in Turkey. Additionally, we explored the correlation between JCPyV presence, immunological parameters, and demographic factors, providing the first molecular epidemiological report of JCPyV in this population. A prospective, multicentre, cross-sectional study was conducted on 107 PLWH and 77 healthy controls. JCPyV DNA was detected and quantified using qPCR, and VP1 gene sequencing was performed to determine viral genotypes. Phylogenetic analysis was conducted using Clustal Omega and the Neighbour-Joining method with a bootstrap value of 1000.

Results: JCPyV viruria was detected in 46% of PLWH and 18.18% of healthy individuals, with no significant association between viruria frequency and immunodeficiency severity (p > 0.05). Genotype IV was the most prevalent (37.5%), followed by Genotype I (31.25%) and Genotype II (31.25%), aligning with European epidemiological data. No Genotype III was detected. No VP1 mutations associated with PML or immune evasion were identified. However, amino acid substitutions were observed at positions 74, 92, 116, 127, and 133, warranting further investigation.

Conclusion: This study provides the first molecular epidemiological analysis of JCPyV in PLWH from Turkey, demonstrating a genotype distribution consistent with European data. While no significant PML-associated VP1 mutations were detected, the identification of substitutions underscores the need for continued molecular surveillance. Understanding JCPyV genotype dynamics and immune evasion strategies is crucial for developing targeted therapeutics, including VP1-based vaccines and monoclonal antibody treatments for high-risk populations.

During the COVID-19 pandemic, neuropsychiatric disorders began to be observed in a significant proportion of patients, occurring at different times after infection and characterised by varying degrees of severity. This article discusses neurological and psychiatric disorders associated with SARS-CoV-2 virus infection, taking into account biological pathomechanisms and psychosocial factors. The long COVID-19 along with the "brain fog" phenomenon were considered in the study. The purpose of the study is to analyse and discuss the available information from the scientific literature on the possible association between SARS-CoV-2 virus infection and the occurrence of neuropsychiatric disorders with different degrees of severity and temporal correlation. To discuss the correlation of COVID-19 with the occurrence of neuropsychiatric disorders, a systematic literature review was conducted using the following databases: PubMed, Elsevier and Google Scholar. The following keywords were used when searching the materials used: "neuropsychiatric disorders", "COVID-19", "SARS-CoV-2", "NeuroCOVID", "cytokine storm" and "long COVID-19". Focusing on the characteristics of the materials and methods used, as well as the results obtained and conclusions reached in each article, 164 publications of research, meta-analysis, review and case reports were included in the study. Neuropsychiatric disorders resulting from SARS-CoV-2 virus infection are multifactorial in nature. The main elements responsible for the varied pattern of symptoms include direct and indirect central nervous system effects of the disease, individual patient conditions, psychosocial factors, severity of immune responses and severity of infection. The neuropsychiatric effects of SARS-CoV-2 infection can be divided into symptoms directly related to the neurological and psychiatric zones and mixed disorders.

Background: Human herpesviruses (HHVs) are lifelong pathogens that can reactivate under stress or immunological changes. Depression has been implicated as both a potential trigger for and a consequence of HHV reactivation. This study investigates the bidirectional relationship between HHV reactivation and depression through a systematic review and meta-analysis.

Methods: This systematic review and meta-analysis followed PRISMA guidelines and was registered in PROSPERO (CRD42024565616). A search of PubMed, Web of Science, Embase, and Scopus identified studies published through March 5, 2024.

Results: Nineteen studies, representing a total sample size of 94,194 participants, were included in the meta-analysis. The pooled odds ratio (OR) demonstrated a significant association between HHV reactivation and depression (OR = 1.33; 95% CI: 1.07-1.64; p < 0.001; I² = 92%). Subgroup analyses revealed significant associations for Epstein-Barr virus (EBV) (OR = 1.99; 95% CI: 1.80-2.20) and herpes simplex virus 2 (HSV-2) (OR = 1.83; 95% CI: 1.32-2.55), while cytomegalovirus (CMV) and HSV-1 showed non-significant associations. A secondary meta-analysis found a significant association between pre-morbid depression and EBV reactivation (OR = 2.18; 95% CI: 1.48-3.21) as well as varicella-zoster virus (VZV) reactivation (HR = 1.09; 95% CI: 1.06-1.13). Sensitivity analyses confirmed the robustness of the findings, and no substantial publication bias was detected.

Conclusion: This study provides evidence of a bidirectional relationship between HHV reactivation and depression, highlighting depression as both a risk factor for and a potential consequence of HHV reactivation.