The link between human herpesvirus 8 (KSHV) and Kaposi's Sarcoma (KS) has been proven, but many important aspects including risk factors, genetic predisposition to tumor development, transmission of KHSV, and the pathogenic potential of different genotypes remain to be elucidated.Possible associations between clinical parameters and antibody levels, viral load fluctuations, and viral genotype were analyzed by quantitative real-time PCR, an in-house developed IFA assay, and sequence analysis of ORF K1-VR1 in blood, serum and saliva of 38 subjects with classic KS (cKS). KHSV lytic antibodies were significantly increased in stage IV compared to stage I and II patients (p= 0.006 and p=0.041, respectively). KHSV blood, serum, and saliva viral load was comparable in all stages. The highest viral loads were detected in saliva, and they decreased in stage III-IV compared to stage I-II patients. Higher concentrations of lytic antibodies and higher viral loads were observed in fast progressing cKS patients, in whom KHSV detection from blood was also more frequent. Type A KSHV strain was almost exclusively present in fast progressors (12/17 cases), while C type was mainly present in slow progressing patients (6/7 cases). Finally, detection of type A KHSV strain associated with higher blood viral loads.KHSV lytic antibody levels and viral load can be used to monitor clinical evolution of cKS. Infection supported by KHSV A subtype is associated with faster progressing disease. Careful monitoring and aggressive therapeutic protocols should be considered in patients with KHSV A-supported infection.

Human polyomavirus JC (JCV) infects the worldwide population, remains latent in the kidney, and is excreted in the urine. A longitudinal study was performed in order to evaluate JCV excretion, to characterize molecularly the virus and to determine if its presence in urine is a consequence of viral reactivation or merely of epithelial squamous cell shedding. The presence of cellular sediment and the JCV genome were examined in 333 urine samples collected periodically for 3 months from 17 healthy subjects; molecular characterization, and quantitation of the virus were also undertaken. JCV DNA was detected in 40.2% of the samples, with a significant difference (P<0.001) observed between males and females. JCV shedding was independent of the presence of cellular sediment in every individual. JCV genotype 1 was the genome detected most frequently, while all of the amplified strains showed archetypal organization of the transcriptional control region (TCR). No clinical symptoms have been associated with JCV excretion and no microbial load was detected in the urine samples. The lack of correlation between JCV DNA detection and the presence of squamous cells in urine sediment indicates that viruria is regulated by the life cycle of JCV. Thus, the virus is eliminated as consequence of its reactivation.

The Delta variant of concern of severe acute respiratory syndrome coronavirus 2 is dominant worldwide. We report a case cluster caused by Delta sublineage B.1.617.2 harboring the mutation E484K in Italy during July 11–July 29, 2021. This mutation appears to affect immune response and vaccine efficacy; monitoring its appearance is urgent.

This is a case study of a child who developed roseola infantum first, then varicella, and was later affected by acute cerebellar syndrome, severe truncal ataxia, and myoclonic dystonia. Human herpesvirus 6 (HHV-6) A and B were detected in the cerebrospinal fluid (CSF) and peripheral blood, respectively, upon ataxia onset. The intricacy of this case suggests multifaceted conclusions ranging from the need for a multidirectional approach to neurological diseases, to confirmation of a more pronounced neurotropism of HHV-6A and a possible role of viruses in myoclonic dystonia syndrome, although this last hypothesis should be confirmed by larger studies.