Adult with Coxsackie B virus-induced cardiomyopathy presents rare case of complicated acute embolic ischaemic stroke.

Introduction and importance: Stroke, a global health concern, often results from embolic events of cardiac origin. Coxsackie B virus (CBV) myocarditis, a common cause of viral heart infections, can lead to cardiac thrombi formation, subsequently causing devastating complications such as embolic stroke. The authors present a rare case of a 26-year-old male who experienced an embolic stroke following CBV myocarditis and cardiomyopathy. Case presentation: The patient exhibited left-sided weakness, facial droop, and respiratory distress. Laboratory findings indicated leukocytosis, hyponatremia, and elevated troponin I. Imaging revealed an acute right basal ganglia infarct and multifocal pulmonary embolism. The diagnosis involved positive CBV serology, severely reduced left ventricular function, and a large apical thrombus. Discussion: Cardioembolic strokes, often attributable to atrial fibrillation, can also result from intracardiac thrombosis associated with myocarditis. CBV, implicated in up to 40% of acute myocarditis cases, binds to cardiac myocytes, triggering inflammation and potential thrombus formation. Myocarditis-induced hypercoagulability increases the risk of thromboembolic events, complicating the clinical course. Conclusion: CBV myocarditis poses a risk of heart failure, cardiomyopathy, and thromboembolic complications such as embolic stroke. Vigilant monitoring for complications and prompt management is crucial, as primary disease treatment remains primarily supportive. This case highlights the need for increased awareness and further studies to understand the intricate relationship between viral myocarditis and embolic strokes.

An Atypical Presentation of Viral Myocarditis Masquerading as Non-ST-Elevation Myocardial Infarction (NSTEMI).

Coxsackie B virus is primarily associated with fever, pharyngitis, and gastrointestinal symptoms, while myocarditis is rarely reported. We present a rare case of a 47-year-old male with a history of hypertension and obesity, who developed Coxsackie B virus-induced myositis, myocarditis, and polyarthralgia. The patient presented with worsening back pain radiating to his chest, migratory arthralgia, exertional dyspnea, and bilateral shoulder pain with arm weakness. Initial investigations revealed elevated creatinine kinase (CK) levels and troponin I, alongside a high white blood cell (WBC) count and C-reactive protein (CRP) levels. Given the patient's symptoms and uptrending troponin without EKG changes, there was a high concern for non-ST-elevation myocardial infarction (NSTEMI), leading to initial treatment with aspirin and IV heparin. However, further questioning revealed a recent sore throat and contact with an ill family member, prompting investigations for an infectious etiology. A viral panel confirmed Coxsackie B virus infection. The patient made a full recovery with supportive care. This case highlights the importance of considering viral causes, particularly the Coxsackie B virus, in patients presenting with muscle pain, cardiac symptoms, and joint pain. Comprehensive viral testing is crucial for early identification and appropriate management to prevent long-term complications. Understanding the mechanisms of Coxsackie B virus infection is essential for developing effective treatment strategies addressing both the viral infection and the inflammatory response.

Steroid-Responsive Seronegative Immune-Mediated Necrotizing Myopathy Likely Triggered by Coxsackie B Virus: A Case Report.

Viral myositis can be mistaken for other types of myopathies, and the main causes of muscle damage are direct myotoxic effect and immune-mediated mechanisms. The biochemical parameters, electromyography (EMG), and muscle biopsy findings can be similar in viral myositis and idiopathic inflammatory myopathies. Viruses are rarely isolated from muscle biopsy specimens, so clinical evaluation and ancillary tests are necessary for a definitive diagnosis. Viral etiology is suspected when weakness occurs after a respiratory or gastrointestinal infection. Coxsackieviruses, particularly A9 and B5, can cause myositis and muscle necrosis. This is a case of a 47-year-old female with a history of alcoholic cirrhosis and a recent coxsackie B virus infection presented with weakness, numbness, and body pain. Creatine kinase levels were elevated but tests for extended myositis panel and antibodies were negative. A muscle biopsy revealed immune-mediated inflammatory myopathy. After a week without improvement, the patient received IV methylprednisolone followed by prednisone taper leading to improvement in symptoms. Prolonged myalgia has been observed in patients recovering from coxsackie A infections. The role of coxsackie B in causing myositis is still disputed and requires more reported data and guidelines. Clinicians should consider testing for coxsackie B as a potential cause of weakness. Awareness of potential complications like myositis can aid in effective patient management. More cases are needed to determine the significance of steroid use in managing coxsackie B-related muscle weakness.

Coxsackie B virus myositis in a healthy young man with mumps co-infection.

Infection is an established but uncommon etiology of myositis, and Coxsackie B virus has only been rarely described as a causative agent. We present a case of a 38-year-old male who presented with weakness, myalgias, and testicular pain following two weeks of upper respiratory infection. Laboratory tests revealed an elevated creatine kinase and positive serology for Coxsackie B4 and mumps. This unusual presentation of Coxsackie B myositis and mumps co-infection in a previously healthy young patient illustrates the importance of including infectious etiologies in the differential diagnosis and the potential life-threatening consequences of biased clinical reasoning.

Coxsackie B Virus-Induced Cardiac Tamponade and Adrenal Insufficiency.

We report a case involving a young male patient without a significant medical history who exhibited symptoms of fatigue, shortness of breath, chest and back pain, and syncope with vomiting. He was found to have adrenal insufficiency and cardiac tamponade requiring pericardiocentesis. Further inpatient workup revealed the patient had positive IgM and IgG antibody titers for the coxsackie B virus, which we believe caused his presentation. The coxsackie B virus strain can cause mild gastrointestinal to more severe cardiac and neurological complications, including meningitis and myocarditis. On rare occasions, the virus can appear in an unexpected fashion, such as in cardiac tamponade or hormonal disruption. This case raises attention to the broad manifestations of the virus and recognizing its more uncommon presentations.

Unusual Presentation of Coxsackievirus B and Methicillin-Sensitive Staphylococcus aureus Cellulitis Causing Sepsis.

The clinical association between Coxsackievirus B (CVB) and methicillin-sensitive Staphylococcus aureus (MSSA) has not been well established in the current literature. Here, we report a case of a 29-year-old male who presented with fever and malaise 24 hours after noticing a pruritic lesion on the anterior foreleg that resembled a mosquito bite. After multiple ED visits, laboratory studies, and imaging tests, the patient was admitted for treatment of high fevers and pancytopenia. The final diagnosis was viral sepsis complicated by co-infection with MSSA.

Dilated Cardiomyopathy as a Result of Coxsackie B Virus Myocarditis.

Dilated cardiomyopathy (DCM) is a myocardial disease that is characterized by left ventricular or biventricular dilation and impairment of systolic function. The etiology is often unknown although it has been thought that DCM may be a consequence of viral myocarditis. The most commonly implicated viruses in the development of myocarditis include coxsackie B virus, hepatitis, parvovirus, cytomegalovirus, influenza virus, and adenovirus. DCM carries a poor prognosis and high rates of mortality, therefore early diagnosis and treatment are imperative. A 47-year-old male presented with atypical chest pain, along with progressive dyspnea. The patient also endorsed symptoms consistent with acute viral syndrome roughly one week prior to presenting to the hospital. The patient initially presented in cardiogenic shock. An initial workup including an echocardiogram was done and showed an ejection fraction of 10-15% with severe left ventricular and left atrial dilation. Left-sided cardiac catheterization revealed nonobstructive coronary artery disease. The patient was placed on mechanical circulatory and inotropic support and was transferred to the cardiovascular intensive care unit. Cardiac MRI was done and showed a moderately sized pericardial effusion along with signs indicative of myocarditis. Serologic testing was positive for coxsackie B virus type IV antibodies. The patient's clinical picture improved as circulatory and inotropic support was removed and the patient was discharged with close outpatient follow-up and evaluation for cardiac transplant.

Coxsackie B viral infection presenting with hemorrhagic pericardial effusion and pleural effusion.

We report an 11-year-old female child presenting with hemorrhagic pericardial effusion causing cardiac tamponade along with moderate left ventricular dysfunction, who screened positive for Coxsackie B infection in the setting of cough, shortness of breath, and chest pain. She needed emergency pericardiocentesis. She also had massive bilateral hemorrhagic pleural effusions requiring bilateral chest drains placement. With a presumed diagnosis of acute myopericarditis, she was treated with steroids and ibuprofen. She made a full recovery without any further recurrence of pericardial or pleural effusion.

Synthesis, antiviral, DFT and molecular docking studies of some novel 1,2,4-triazine nucleosides as potential bioactive compounds.

A novel series of nucleosides with potential antiviral activity have been synthesized and characterized using IR, MS, 1D NMR and 2D NMR data. The antiviral activity of the synthesized compounds was assessed against the Coxsackie B virus and Hepatitis A virus (HAV-10). The results revealed that compound 6 is equipotent to the standard drug Ribavirin against HAV-10. Also, some computational studies, such as the prediction of pharmacokinetic properties, toxicity, and bioactivity, have been done.

Antiviral activity of castor oil plant (Ricinus communis) leaf extracts.

ETHNOPHARMACOLOGICAL RELEVANCE: Ricinus communis L., commonly known as castor oil plant, is a precious traditional medicine with a history of thousands of years in the world. Castor oil plant has high traditional and medicinal values for treating liver infections, stomach ache, flatulence, constipation, inflammation, warts, colic, enteritis, fever, headache, and as a counter irritant. Its diverse phytochemicals have a wide range of valuable medicinal activities including hepatoprotective, anti-nociceptive, antioxidant, antiulcer, anticancer, anti-inflammatory, central analgesic, antidiabetic, antimicrobial, antiviral, and wound healing activity. AIM OF THE WORK: To provide a complete characterization of the composition of Ricinus communis leaves using ultra-performance liquid chromatography coupled with hybrid triple time-of-flight mass spectrometry (UPLC-Triple TOF-MS/MS) and different chromatographic techniques and to evaluate its antiviral potential using three mechanisms against three common viruses. MATERIALS AND METHODS: R. communis leaves were extracted with 70% methanol and further partitioned with solvents of increasing polarities: petroleum ether, dichloromethane (CH2Cl2), ethyl acetate, and n-butanol. The CH2Cl2 and n-butanol fractions were subjected to repeated chromatographic separation to isolate the phytochemicals, and their structures were elucidated using nuclear magnetic resonance spectroscopy. UPLC-Triple TOF-MS/MS was performed to determine the different phytochemicals in the ethyl acetate fraction. The antiviral activity of the extracts was investigated using the maximum nontoxic concentration of each against the challenge dose of the virus (CDV) and 1/10 and 1/100 dilutions of the CDV for Coxsackie B virus type 4 (COXB4), herpes simplex virus type 1 (HSV1), and hepatitis A virus (HAV) using Vero cell cultures that were treated according to three protocols to test for anti-replicative, protective, and anti-infective antiviral activity. Cell viability was evaluated using the MTT colorimetric assay and each experiment is repeated three times independently of each other. RESULTS: R. communis leaves possessed antiviral activity. Evaluation of the anti-replicative activity showed that all extracts possessed high anti-replicative activity against HAV especially methanol and methylene chloride fractions and moderate activity against COXB4; butanol > methylene chloride and ethyl acetate > methanol. All extracts showed protective activity against HAV, especially butanol extract, while methanol extracts showed higher non-significant antiviral protective activity against HSV1 vs Acyclovir. Almost no anti-infective effects were recorded for any extract against the studied viruses. CONCLUSION: The discriminatory effect against each virus by different mechanisms suggests the presence of different chemical compounds. The alkaloid and phenolic derivatives of the extracts of R. communis leaves may help develop a drug to prevent or treat common viral infections. Further investigations are recommended to define the bioactive antiviral properties of R. communis leaves.

Proteomic and Transcriptional Profiles of Human Stem Cell-Derived ß Cells Following Enteroviral Challenge.

Enteroviral infections are implicated in islet autoimmunity and type 1 diabetes (T1D) pathogenesis. Significant ß-cell stress and damage occur with viral infection, leading to cells that are dysfunctional and vulnerable to destruction. Human stem cell-derived ß (SC-ß) cells are insulin-producing cell clusters that closely resemble native ß cells. To better understand the events precipitated by enteroviral infection of ß cells, we investigated transcriptional and proteomic changes in SC-ß cells challenged with coxsackie B virus (CVB). We confirmed infection by demonstrating that viral protein colocalized with insulin-positive SC-ß cells by immunostaining. Transcriptome analysis showed a decrease in insulin gene expression following infection, and combined transcriptional and proteomic analysis revealed activation of innate immune pathways, including type I interferon (IFN), IFN-stimulated genes, nuclear factor-kappa B (NF-κB) and downstream inflammatory cytokines, and major histocompatibility complex (MHC) class I. Finally, insulin release by CVB4-infected SC-ß cells was impaired. These transcriptional, proteomic, and functional findings are in agreement with responses in primary human islets infected with CVB ex vivo. Human SC-ß cells may serve as a surrogate for primary human islets in virus-induced diabetes models. Because human SC-ß cells are more genetically tractable and accessible than primary islets, they may provide a preferred platform for investigating T1D pathogenesis and developing new treatments.

Autophagy Proteins in Viral Exocytosis and Anti-Viral Immune Responses.

Abstract: Autophagy-related (Atg) gene-encoded proteins were originally described for their crucial role in macroautophagy, a catabolic pathway for cytoplasmic constituent degradation in lysosomes. Recently it has become clear that modules of this machinery can also be used to influence endo- and exocytosis. This mini review discusses how these alternative Atg functions support virus replication and viral antigen presentation on major histocompatibility (MHC) class I and II molecules. A better understanding of the modular use of the macroautophagy machinery might enable us to manipulate these alternative functions of Atg proteins during anti-viral therapies and to attenuate virus-induced immune pathologies.

miR-466 is putative negative regulator of Coxsackie virus and Adenovirus Receptor.

This study aimed at elucidating how Coxsackie B virus (CVB) perturbs the host's microRNA (miRNA) regulatory pathways that lead to antiviral events. The results of miRNA profiling in rat pancreatic cells infection models revealed that rat rno-miR-466d was up-regulated in CVB infection. Furthermore, in silico studies showed that Coxsackie virus and Adenovirus Receptor (CAR), a cellular receptor, was one of the rno-miR-466d targets involved in viral entry. Subsequent experiments also proved that both the rno-miR-466d and the human hsa-miR-466, which are orthologs of the miR-467 gene family, could effectively down-regulate the levels of rat and human CAR protein expression, respectively.

Programmed necrosis in microbial pathogenesis.

Programmed cell death is an important facet of host-pathogen interactions. Although apoptosis has long been implicated as the major form of programmed cell death in host defense, the past decade has seen the emergence of other forms of regulated death, including programmed necrosis. While the molecular mechanisms of programmed necrosis continue to be unveiled, an increasing number of viral and bacterial pathogens induce this form of death in host cells, with important consequences for infection, control, and pathogenesis. Moreover, pathogen strategies to manipulate or utilize this pathway are now being discovered. In this review, we focus on a variety of viral and bacterial pathogens where a role for programmed necrosis is starting to be appreciated. In particular, we focus on the mechanistic details of how the host or the pathogen might appropriate this pathway for its own benefit.

Tropism Analysis of Two Coxsackie B5 Strains Reveals Virus Growth in Human Primary Pancreatic Islets but not in Exocrine Cell Clusters In Vitro.

Human Enteroviruses (HEVs) have been implicated in human pancreatic diseases such as pancreatitis and type 1 diabetes (T1D). Human studies are sparse or inconclusive and our aim was to investigate the tropism of two strains of Coxsackie B virus 5 (CBV-5) in vitro to primary human pancreatic cells. Virus replication was measured with TCID50 titrations of aliquots of the culture medium at different time points post inoculation. The presence of virus particles or virus proteins within the pancreatic cells was studied with immunohistochemistry (IHC) and electron microscopy (EM). None of the strains replicated in the human exocrine cell clusters, in contrast, both strains replicated in the endocrine islets of Langerhans. Virus particles were found exclusively in the endocrine cells, often in close association with insulin granules. In conclusion, CBV-5 can replicate in human endocrine cells but not in human exocrine cells, thus they might not be the cause of pancreatitis in humans. The association of virus with insulin granules might reflect the use of these as replication scaffolds.

Antenatal and postnatal diagnosis of coxsackie b4 infection: case series.

Enteroviruses are a common cause of neonatal infection. In particular, Coxsackie B viruses are often associated with severe, fatal disease. The antenatal diagnosis of Coxsackie B viral infections is uncommon. We present a unique case of Coxsackie B4 virus ventriculitis and myocarditis causing fetal hydrops at 22 weeks gestation. Transmission was inferred by viral isolation from the amniotic fluid and by placental pathology. We also describe two additional cases of fatal neonatal Coxsackie B4 infection complicated by myocarditis and encephalitis with cerebral necrosis in a 4-day-old female and by myocarditis, spinal leptomeningitis, and hepatitis in a 4-day-old male. Transplacental acquisition of infection carries a poor prognosis. We propose that Coxsackie B virus should be considered in the investigation of nonimmune hydrops, particularly in the presence of cardiac dysfunction.