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We isolated five mAbs with potent neutralizing activities against SARS-CoV-2 from two convalescent COVID-19 patients infected with prototype virus. Among them, the 9-105 antibody that have a highest affinity for the receptor-binding domain (RBD), cross-neutralize variants, such as B.1.1.7 (alfa), mink cluster 5 variant, B.1.351 (beta), P.1 (gamma), C.37 (lambda), B.1.617.1 (kappa), B.1.617.2 (delta) and B.1.621 (mu). A single amino acid mutation at K417 of RBD decreased neutralization sensitivity of 9-105. A 9-105 homology model revealed that 9-105 light chain binds to RBD including K417 by the same angle as ACE2.

Antibodies against the receptor binding domain of the spike protein of SARS-CoV-2 play an important role in preventing infection as neutralizing antibodies. However, antibodies that recognize a specific site on the N-terminal domain of the spike protein induce an open domain of receptor binding that increases the binding of ACE2 and enhances the infectivity of SARS-CoV-2. Furthermore, the presence of the infectivity-enhancing antibodies reduces the neutralizing activity of the neutralizing antibodies. Therefore, when considering the antibody response to SARS-CoV-2, it is necessary to consider not only neutralizing antibodies but also the balance between neutralizing and infectivity-enhancing antibodies. In this article, function and mechanism of infectivity-enhancing antibodies are introduced.

013-2016 Ebola virus disease (EVD) outbreak was the largest EVD outbreak ever documented that started earlier in Guinea and later widely spread throughout West Africa, ending up a total of > 28,000 human infections. In this review, we outline research findings on Ebola virus (EBOV) variant Makona, a new EBOV variant isolated from the 2013-2016 EVD outbreak, and introduce the unique biological and pathogenic characteristics of Makona variant. We also discuss about the relevance of persistent infection of EBOV in EVD survivors with resurgence of EVD outbreak in Guinea in 2021. Moreover, this review covers a recent case report of EVD relapse and deliberates new interpretations of EBOV biology and EVD outbreak.

A new etiological agent of an acute febrile illness following tick bite has been found in Hokkaido, Japan, in 2019 and designated as Yezo virus. Seven cases of Yezo virus infection were identified from 2014 to 2020 by passive and retrospective surveillance. Yezo virus is classified into the genus Orthonairovirus, family Nairoviridae and forms Sulina genogroup together with Sulina virus, which was identified in ticks in Romania. The Sulina genogroup viruses are closely related to the Tamdy genogroup viruses recently reported as causative agents of febrile illness in China and distant from known orthonairovirus pathogens, such as Crimean-Congo hemorrhagic fever virus. Since only limited information is available for the emerging orthonairovirus diseases, including Yezo virus infection, their occurrence should be carefully monitored.

Influenza viruses utilize sialic acid-containing glycoconjugates as receptors. The distribution of receptors in host tissues has been investigated in many species to understand the ecology of influenza viruses in nature and the mechanisms of interspecies transmission of the viruses. On the other hand, lectins, which have been widely used to detect these receptor molecules, have many different characteristics from antibodies and thus, require special attention in interpreting the results of lectin staining. In particular, lectins derived from Maackia amurensis, which has been used to detect Siaα2-3Gal, the avian-type receptor for influenza viruses, have been used without fully understanding its characteristics. This led to some confusion in interpreting the distribution of influenza virus receptors in host tissues. How accurately do we know the distribution of avian-type receptors in host animals? In this article, we would like to suggest reviewing the influenza virus receptors by providing issues related to Maackia lectins.

In healthcare facilities, the initial response to emerging and reemerging infectious diseases, including COVID-19, requires systematic management. The first step is to establish an initial risk assessment and subsequent response flow, using a combination of triage and clinical examination for patients. Screening tests are performed for the early diagnosis of asymptomatic patients who are judged to be at low risk in the initial assessment. However, regardless of the test results, subsequent patient care should be taken cautiously to avoid inadequate initial evaluation at the time of admission, follow-up of symptoms and infection control measures after admission. The basic principle is standard precautions, with particular emphasis on compliance with hand hygiene. Universal masking for preventing transmission from asymptomatic/pre-symptomatic patients and reducing droplet emission and inhalation become the new essential precaution. For suspected/confirmed patients with COVID-19, surgical mask or N95 mask, gloves, gown, eye protection, and cap are basically used. The policy for personal protective equipment is made based on the medical environment of each facility. A negative pressure room is not always required but should be considered in high-risk environments, if possible. While the risk of transmission from the surface environment in a standard healthcare delivery system is limited, a continuous review of the facility environment is expected, considering the importance of ventilation.

B virus is a herpes virus that natutaly infects macaque monkeys. It is extremely neuropathogenic when infection occurs in humans. B virus infection has been reported only in laboratory workers and breeders of macaque monkeys in North America and the United Kingdom, and it is therefore recognized as a rare infectious disease. The first cases of B virus disease were reported in Japan in 2019 and in China in 2021, although no cases had been reported since 1997. Although B virus disease has not been reported for more than 20 years, the potential threat has always existed. The viral factors responsible for the strong neuropathogenicity of B virus to humans has not been identified. There are no reports of infection by contact with wild macaque monkeys, but the possibility can not been ruled out. In this paper, we describe its virological properties, findings from B virus disease from patient-reported cases, and the genotype of B virus.