Cognitive decline and poor social relationship in older adults during COVID-19 pandemic: can information and communications technology (ICT) use helps?

BACKGROUND: To answer whether older adults' cognitive function benefits from ICT use, we (1) examined the relationship between ICT use and cognitive decline during the COVID-19 pandemic and (2) explored the potential role of ICT use in mitigating the relationship between loneliness, social isolation, and cognitive decline among community-dwelling older adults. METHODS: From February to March 2021, a mail survey was distributed to 1,400 older adults aged 70-89 years old. Responded participants were 1,003 (71.6% response rate). Subjective cognitive decline (SCD) was the independent variable. ICT use was assessed based on ICT use history and current ICT use activities. Loneliness was based on the Japanese version of the Three-Item Loneliness Scale. Social isolation was a total score of six items. Covariate-adjusted logistic regressions were performed and stratified by age groups (70-79 and ≥ 80 years). RESULTS: During the COVID-19 epidemic, the proportion of people aged ≥ 80 years who reported cognitive decline was twice that of 70s. Non-ICT use was independently associated with a higher risk of cognitive decline in participants aged ≥ 80 years. Furthermore, the significant associations between cognitive decline and interaction items (non-ICT use by loneliness or social isolation) were observed in the ≥ 80 age group. No association was found in the 70-79 age group. CONCLUSIONS: Non-ICT users with high loneliness or social isolation scores were more likely to experience cognitive decline for adults age ≥ 80 years. For older adults who were vulnerable to poor social relationships, ICT use is potentially an efficient intervention. Further longitudinal investigations are needed.

Lipoprotein Receptors Redundantly Participate in Entry of Hepatitis C Virus.

Scavenger receptor class B type 1 (SR-B1) and low-density lipoprotein receptor (LDLR) are known to be involved in entry of hepatitis C virus (HCV), but their precise roles and their interplay are not fully understood. In this study, deficiency of both SR-B1 and LDLR in Huh7 cells was shown to impair the entry of HCV more strongly than deficiency of either SR-B1 or LDLR alone. In addition, exogenous expression of not only SR-B1 and LDLR but also very low-density lipoprotein receptor (VLDLR) rescued HCV entry in the SR-B1 and LDLR double-knockout cells, suggesting that VLDLR has similar roles in HCV entry. VLDLR is a lipoprotein receptor, but the level of its hepatic expression was lower than those of SR-B1 and LDLR. Moreover, expression of mutant lipoprotein receptors incapable of binding to or uptake of lipid resulted in no or slight enhancement of HCV entry in the double-knockout cells, suggesting that binding and/or uptake activities of lipid by lipoprotein receptors are essential for HCV entry. In addition, rescue of infectivity in the double-knockout cells by the expression of the lipoprotein receptors was not observed following infection with pseudotype particles bearing HCV envelope proteins produced in non-hepatic cells, suggesting that lipoproteins associated with HCV particles participate in the entry through their interaction with lipoprotein receptors. Buoyant density gradient analysis revealed that HCV utilizes these lipoprotein receptors in a manner dependent on the lipoproteins associated with HCV particles. Collectively, these results suggest that lipoprotein receptors redundantly participate in the entry of HCV.

Biological and immunological characteristics of hepatitis E virus-like particles based on the crystal structure.

Hepatitis E virus (HEV) is a causative agent of acute hepatitis. The crystal structure of HEV-like particles (HEV-LP) consisting of capsid protein was determined at 3.5-A resolution. The capsid protein exhibited a quite different folding at the protruding and middle domains from the members of the families of Caliciviridae and Tombusviridae, while the shell domain shared the common folding. Tyr-288 at the 5-fold axis plays key roles in the assembly of HEV-LP, and aromatic amino acid residues are well conserved among the structurally related viruses. Mutational analyses indicated that the protruding domain is involved in the binding to the cells susceptive to HEV infection and has some neutralization epitopes. These structural and biological findings are important for understanding the molecular mechanisms of assembly and entry of HEV and also provide clues in the development of preventive and prophylactic measures for hepatitis E.

Production of hepatitis E virus-like particles presenting multiple foreign epitopes by co-infection of recombinant baculoviruses.

Hepatitis E virus (HEV) causes not only endemics via a fecal-oral route but also sporadic cases via zoonotic transmission or blood transfusion. HEV-like particles (HEV-LP) produced by using a baculovirus expression system are considered a candidate for mucosal vaccines for HEV infection. In this study, we attempted to produce a chimeric HEV-LP presenting various foreign epitopes on its surface. Expression of the recombinant capsid proteins carrying a myc- or FLAG-tag inserted between amino acid residues 488 and 489, which are located in the exterior loop on the protruding domain of the HEV capsid, resulted in the production of recombinant HEV-LP. Although expression of the recombinant capsid protein carrying the HA-tag inserted at the same site failed to produce any particles, co-expression with the myc-tagged capsid protein successfully yielded a chimeric HEV-LP consisting of both recombinant capsid proteins. Immunoprecipitation analyses confirmed that the chimeric particles present these foreign epitopes on the surface. Similar results were obtained for the expression of the recombinant capsid proteins carrying neutralizing epitopes of Japanese encephalitis virus. These results suggest the chimeric HEV-LP system provides a novel vaccine carrier that can accommodate multiple neutralizing epitopes on its surface.