Seasonal distribution was seen for each virus. There were no significant differences in clinical symptoms in the children studied. Because the infection of rhinoviruses is the common occurrence in children, it is hypothesized that the factors related to disease severity are mainly the underlying conditions of the children.

ABSTRACT. Cell-mediated and humoral immune responses are attenuated with aging. Intracellular glutathione (GSH) levels also decrease with aging. Previously, we have reported that combined administration of L -cystine and L -theanine enhances antigen-specific IgG production, partly through augmentation of GSH levels and T helper 2-mediated responses in 12-week-old mice. These findings suggest that combined administration of L -cystine and L -theanine to aged mice improves immune responses via increase of GSH synthesis. Here, we examined the effects of combined administration of L -cystine and L -theanine on antigen-specific antibody production and influenza virus infection in aged mice. Combined administration of these amino acids for 14 days before primary immunization significantly enhanced the serum antigen-specific IgM and IgG levels in 24-month-old mice. Furthermore, 13-month-old mice co-treated with these amino acids orally for 10 days had significantly lower lung viral titers than controls at 6 days after influenza virus infection. In addition, this co-treatment also significantly prevented the weight loss associated with infection. Enhancement of anti-influenza-virus IgG antibodies by combined administration of L -cystine and L -theanine was seen 10 days after infection. The significantly elevated serum interleukin-10/interferon- ratio and -glutamylcysteine synthetase mRNA expression, which is the rate-limiting enzyme of GSH synthesis, in the spleen 3 days after infection may have contributed to the observed beneficial effects. These results suggest that combined administration of L -cystine and L -theanine enhances immune function and GSH synthesis which are compromised with advanced age, and may become a useful strategy in healthy aging. With aging, the human body's defense capability weakens, including production of antibodies and cytotoxic T lymphocytes (CTL) and cellular immune function [12,28]. These age-related alterations seem to result from oxidative stress [9]. Diet supplementation with antioxidants has been used to prevent or delay the onset of age-related immune impairment [7]. For example, a diet that contains the antioxidant 2-mercaptoethanol, which reduces cystine to cysteine and increases the intracellular concentration of glutathione (GSH; L --glutamyl-L -cysteinyl-glycine), improves several types of immune response in aged mice [17]. Dietary supplementation with GSH, another antioxidant, has also been shown to increase cell-mediated immunity in aged mice [11]. In addition, GSH levels and the gene expression of -glutamylcysteine synthetase (GCS), the rate-limiting enzyme in GSH synthesis, are known to decrease with aging [24]. These results suggest that GSH antioxidant therapy may aid in preventing or delaying the onset of age-related immune impairment.A recent study we performed indicated that combined administration of L -cystine and L -theanine (-glutamylethylamide, a specific amino acid found in green tea) to young mice increases the GSH level in the liver and also enhances the s...

Various viruses of different species were detected in the specimens from the children regardless of their health status. It might be speculated that host factors such as the function of the immune system influence the clinical outcome of the infection. However, this needs to be studied further.

The pandemic caused by a new type of influenza virus, pandemic H1N1 (2009) influenza virus A (AH1pdm), has had a major worldwide impact. Since hemagglutinin (HA) genes are among the most specific genes in the influenza virus genome, AH1pdm can be definitively diagnosed by viral gene analysis targeting the HA genes. This type of analysis, however, cannot be easily performed in clinical settings. While commercially available rapid diagnosis kits (RDKs) based on immunochromatography can be used to detect nucleoproteins (NPs) of influenza A and B viruses in clinical samples, there are no such kits that are specific for AH1pdm. We show here that an RDK using a combination of monoclonal antibodies against NP can be used to specifically detect AH1pdm. The RDK recognized AH1pdm virus isolates but did not recognize seasonal H1N1 and H3N2 and influenza B viruses, indicating that the specificity of the RDK is 100%. A parallel comparison of RDK with a commercial influenza A/B virus kit revealed that both types of kits had equal sensitivities in detecting their respective viruses. Preliminary evaluation of clinical samples from 5 individuals with PCR-confirmed human AH1pdm infection showed that the RDK was positive for all samples, with the same detection intensity as that of a commercial influenza A/B virus kit. This RDK, together with a new vaccine and the stockpiling of anti-influenza drugs, will make aggressive measures to contain AH1pdm infections possible.

During the 1998-1999 influenza season, two distinct influenza B virus Yamagata group strains were isolated from the patients of a private clinic. Each responded differently to monoclonal antibodies (Mabs) 5H4 and 8B3 on staining, and hemagglutination inhibition and neutralizing tests. When the analysis of nucleotide sequences was undertaken, the identity of deduced amino acid sequences of the HA1 region was 94%, which suggested that they derived from different strains. They were termed 5H4-responding strains and 5H4-nonresponding strains, respectively. The analysis of laboratory-induced antigenic variants suggested that the amino acid at position 149 is important to the reactivity to 5H4. This residue was "Arg" in 5H4-responding strains and "Lys" in nonresponding strains. During the 1998-1999 season, a total of 100 influenza B virus strains were isolated and 5H4-responding strains were the major type (94 strains). In the 1999-2000 influenza season, only two influenza B virus strains were isolated. Neither responded to 5H4. However, analysis of the deduced amino acid sequences of the HA1 region suggested that one of the two strains was derived from the 5H4-responding strains of the previous season. The amino acid residue at position 149 was "Lys" in place of "Arg." These observations suggested that 5H4-nonresponding strains will increase in coming seasons.

No abstract

Since the coronavirus disease 2019 (COVID‐19) outbreak, laboratory diagnosis has mainly been conducted using reverse‐transcription polymerase chain reaction (RT‐PCR). Detecting the presence of an infectious virus in the collected sample is essential to analyze if a person can transmit infectious severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). However, there have been no quantitative investigations conducted for infectious SARS‐CoV‐2 in clinical samples. Therefore, in the present study, a rapid and simple focus‐forming assay using the peroxidase‐antiperoxidase technique was developed to quantify infectious SARS‐CoV‐2 titers in 119 samples (n = 52, nasopharyngeal swabs [NPS]; n = 67, saliva) from patients with COVID‐19. Furthermore, the study findings were compared with the cycle threshold (Ct) values of real‐time RT‐PCR. The infectious virus titers in NPS samples and Ct values were inversely correlated, and no infectious virus could be detected when the Ct value exceeded 30. In contrast, a low correlation was observed between the infectious virus titers in saliva and Ct values (r = ‐0.261, p = 0.027). Furthermore, the infectious virus titers in the saliva were significantly lower than those in the NPS samples. Ten days after the onset of COVID‐19 symptoms, the infectious virus was undetectable, and Ct values were more than 30 in NSP and saliva samples. The results indicate that patients whose symptoms subsided 10 days after onset, with Ct values more than 30 in NSP and saliva samples, were less likely to infect others.

SUMMARY: Isolation of novel types of human adenovirus D (HAdV-53, -54, and -56) from keratoconjunctivitis patients has been reported since 2008. We examined the molecular epidemiology of HAdV-D strains using 39 field isolates collected from epidemic keratoconjunctivitis (EKC) patients from 2001 to 2010 in the province of Osaka, Japan. The molecular types were analyzed by sequencing partial penton base gene, loop 1 in the hexon, and complete fiber genes. Of the 39 isolates, the majority were 35.9z) and -37 (13/39, 33.3z), followed by -53 (4/39, 10.3z) and -54 (8/39, 20.5z). Analysis of annual distribution showed that HAdV-19 and -37 were detected before 2004, whereas HAdV-53 and -54 were first identified in 2001 and 2003, respectively, and persistently detected during the study period. It is noted that both HAdV-53 and -54 isolates were misclassified by the serological method. Altogether, the molecular analysis elucidated the epidemiology of HAdV-D and presence of novel types from the early 2000s in Osaka. Further genetic analysis of serologically classified HAdV-D isolates may provide insights into the epidemiology of EKC.