• Keywords
• Varilrix, Varivax, Priorix Tetra, ProQuad,
• MeSH
• Child MeSH
• Herpes Zoster etiology   MeSH
• Contraindications, Procedure MeSH
• Humans MeSH
• Chickenpox * epidemiology   complications   mortality   prevention & control   MeSH
• Post-Exposure Prophylaxis methods   MeSH
• Risk Factors MeSH
• Practice Guidelines as Topic * MeSH
• Chickenpox Vaccine administration & dosage   therapeutic use   MeSH
• Vaccination * methods   MeSH
• Herpesvirus 3, Human MeSH
• Check Tag
• Child MeSH
• Humans MeSH

• MeSH
• Acyclovir pharmacology   therapeutic use   MeSH
• Child MeSH
• Adult MeSH
• Hepatorenal Syndrome etiology   MeSH
• Immunocompromised Host immunology   MeSH
• Blood Coagulation Disorders etiology   immunology   MeSH
• Humans MeSH
• Chickenpox * complications   prevention & control   MeSH
• Chickenpox Vaccine MeSH
• Pneumonia, Viral etiology   drug therapy   MeSH
• Herpesvirus 3, Human * pathogenicity   MeSH
• Check Tag
• Child MeSH
• Adult MeSH
• Humans MeSH
• Male MeSH
• Female MeSH
• Publication type
• Case Reports MeSH

• Keywords
• Shingrix,
• MeSH
• Acyclovir pharmacology   therapeutic use   MeSH
• Vaccines, DNA pharmacology   therapeutic use   MeSH
• Ganglia virology   MeSH
• Herpes Zoster Ophthalmicus * complications   MeSH
• Encephalitis, Varicella Zoster * diagnosis   drug therapy   MeSH
• Virus Latency MeSH
• Humans MeSH
• Magnetic Resonance Imaging, Interventional MeSH
• Vascular Diseases etiology   MeSH
• Aged MeSH
• Herpes Zoster Vaccine MeSH
• Herpesvirus 3, Human MeSH
• Check Tag
• Humans MeSH
• Male MeSH
• Aged MeSH
• Publication type
• Case Reports MeSH

The Ramsay-Hunt syndrome results from reactivation of the varicella-zoster virus at the geniculate ganglion level. The syndrome is characterized by a combination of symptoms such as ipsilateral facial paralysis, otalgia, and vesicles near the ear and auditory canal. The gold standard in the treatment of Ramsay-Hunt syndrome remains the combination of antiviral therapy with corticosteroids and adequate analgesic therapy. We present a case of a 45-year-old patient with severe form of atopic dermatitis, who developed this syndrome during treatment with dupilumab. The risks and benefits of dupilumab treatment in this patient were considered. Because both bronchial asthma and atopic dermatitis worsened when dupilumab was discontinued, it was indicated to continue this therapy with low-dose of acyclovir.

• MeSH
• Acyclovir therapeutic use   MeSH
• Antiviral Agents therapeutic use   adverse effects   MeSH
• Dermatitis, Atopic * drug therapy   MeSH
• Asthma drug therapy   MeSH
• Herpes Zoster Oticus * drug therapy   diagnosis   MeSH
• Antibodies, Monoclonal, Humanized * therapeutic use   adverse effects   MeSH
• Middle Aged MeSH
• Humans MeSH
• Herpesvirus 3, Human MeSH
• Check Tag
• Middle Aged MeSH
• Humans MeSH
• Male MeSH
• Publication type
• Journal Article MeSH
• Letter MeSH
• Case Reports MeSH

Chronic hepatitis B (CHB) remains a major public health problem worldwide, with limited treatment options, but inducing an antiviral response by innate immunity activation may provide a therapeutic alternative. We assessed the cytokine-mediated anti-hepatitis B virus (HBV) potential for stimulating the cyclic GMP-AMP synthase-stimulator of interferon genes (STING) pathway using STING agonists in primary human hepatocytes (PHH) and nonparenchymal liver cells (NPCs). The natural STING agonist, 2',3'-cyclic GMP-AMP, the synthetic analogue 3',3'-c-di(2'F,2'dAMP), and its bis(pivaloyloxymethyl) prodrug had strong indirect cytokine-mediated anti-HBV effects in PHH regardless of HBV genotype. Furthermore, STING agonists induced anti-HBV cytokine secretion in vitro, in both human and mouse NPCs, and triggered hepatic T cell activation. Cytokine secretion and lymphocyte activation were equally stimulated in NPCs isolated from control and HBV-persistent mice. Therefore, STING agonists modulate immune activation regardless of HBV persistence, paving the way toward a CHB therapy.

• MeSH
• Cytokines metabolism   MeSH
• Hepatitis B * drug therapy   MeSH
• Hepatocytes MeSH
• Herpesvirus 1, Cercopithecine * MeSH
• Interferons metabolism   MeSH
• Humans MeSH
• Mice MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Mice MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH

The herpes simplex virus (HSV) is a double-stranded DNA human virus that causes persistent infections with recurrent outbreaks. HSV exists in two forms: HSV-1, responsible for oral herpes, and HSV-2, primarily causing genital herpes. Both types can lead to significant complications, including neurological issues. Conventional treatment, involving acyclovir and its derivatives, faces challenges due to drug resistance. This underscores the imperative for continual research and development of new drugs, with a particular emphasis on exploring the potential of natural antivirals. Flavonoids have demonstrated promise in combating various viruses, including those within the herpesvirus family. This review, delving into recent studies, reveals the intricate mechanisms by which flavonoids decode their antiviral capabilities against HSV. By disrupting key stages of the viral life cycle, such as attachment to host cells, entry, DNA replication, latency, and reactivation, flavonoids emerge as formidable contenders in the ongoing battle against HSV infections.

• MeSH
• Antiviral Agents pharmacology   therapeutic use   MeSH
• Flavonoids pharmacology   therapeutic use   MeSH
• Herpes Simplex * drug therapy   MeSH
• Humans MeSH
• Herpesvirus 1, Human * physiology   MeSH
• Life Cycle Stages MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Review MeSH

• MeSH
• Virus Activation physiology   MeSH
• Data Analysis MeSH
• Herpes Zoster * epidemiology   drug therapy   complications   prevention & control   MeSH
• Disease Notification * MeSH
• Humans MeSH
• Risk Factors MeSH
• Routinely Collected Health Data MeSH
• Vaccination MeSH
• Herpesvirus 3, Human pathogenicity   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Research Support, Non-U.S. Gov't MeSH
• Geographicals
• Czech Republic MeSH

• MeSH
• Virus Activation physiology   MeSH
• Herpes Zoster * epidemiology   complications   prevention & control   MeSH
• Immunogenicity, Vaccine MeSH
• Humans MeSH
• Risk Factors MeSH
• Aged MeSH
• Herpes Zoster Vaccine * economics   pharmacology   immunology   classification   MeSH
• Vaccination economics   MeSH
• Herpesvirus 3, Human pathogenicity   MeSH
• Check Tag
• Humans MeSH
• Aged MeSH
• Publication type
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Geographicals
• Czech Republic MeSH

PURPOSE: The combination of talimogene laherparepvec (T-VEC) and pembrolizumab previously demonstrated an acceptable safety profile and an encouraging complete response rate (CRR) in patients with advanced melanoma in a phase Ib study. We report the efficacy and safety from a phase III, randomized, double-blind, multicenter, international study of T-VEC plus pembrolizumab (T-VEC-pembrolizumab) versus placebo plus pembrolizumab (placebo-pembrolizumab) in patients with advanced melanoma. METHODS: Patients with stage IIIB-IVM1c unresectable melanoma, naïve to antiprogrammed cell death protein-1, were randomly assigned 1:1 to T-VEC-pembrolizumab or placebo-pembrolizumab. T-VEC was administered at ≤ 4 × 106 plaque-forming unit (PFU) followed by ≤ 4 × 108 PFU 3 weeks later and once every 2 weeks until dose 5 and once every 3 weeks thereafter. Pembrolizumab was administered intravenously 200 mg once every 3 weeks. The dual primary end points were progression-free survival (PFS) per modified RECIST 1.1 by blinded independent central review and overall survival (OS). Secondary end points included objective response rate per mRECIST, CRR, and safety. Here, we report the primary analysis for PFS, the second preplanned interim analysis for OS, and the final analysis. RESULTS: Overall, 692 patients were randomly assigned (346 T-VEC-pembrolizumab and 346 placebo-pembrolizumab). T-VEC-pembrolizumab did not significantly improve PFS (hazard ratio, 0.86; 95% CI, 0.71 to 1.04; P = .13) or OS (hazard ratio, 0.96; 95% CI, 0.76 to 1.22; P = .74) compared with placebo-pembrolizumab. The objective response rate was 48.6% for T-VEC-pembrolizumab (CRR 17.9%) and 41.3% for placebo-pembrolizumab (CRR 11.6%); the durable response rate was 42.2% and 34.1% for the arms, respectively. Grade ≥ 3 treatment-related adverse events occurred in 20.7% of patients in the T-VEC-pembrolizumab arm and in 19.5% of patients in the placebo-pembrolizumab arm. CONCLUSION: T-VEC-pembrolizumab did not significantly improve PFS or OS compared with placebo-pembrolizumab. Safety results of the T-VEC-pembrolizumab combination were consistent with the safety profiles of each agent alone.

• MeSH
• Double-Blind Method MeSH
• Humans MeSH
• Herpesvirus 1, Human * MeSH
• Melanoma * drug therapy   MeSH
• Oncolytic Virotherapy * methods   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Clinical Trial, Phase I MeSH
• Clinical Trial, Phase III MeSH
• Multicenter Study MeSH
• Research Support, Non-U.S. Gov't MeSH
• Randomized Controlled Trial MeSH

• MeSH
• Herpes Zoster * etiology   complications   prevention & control   MeSH
• Humans MeSH
• Chickenpox * epidemiology   prevention & control   MeSH
• Neuralgia, Postherpetic diagnosis   MeSH
• Herpes Zoster Vaccine administration & dosage   therapeutic use   MeSH
• Chickenpox Vaccine administration & dosage   therapeutic use   MeSH
• Herpesvirus 3, Human MeSH
• Check Tag
• Humans MeSH