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Nasal obstruction is considered to be one of the risk factors for obstructive sleep apnea, together with a high arched narrow palate, elongated uvula, malocclusion, and tongue and tonsil size. The impact of nasal obstruction on sleep apnea is controversial, however, and its relation to sleep quality is rarely discussed. The purpose of this study was to investigate the independent effect of nasal obstruction on sleep quality.Sixty-nine patients with nasal obstructive symptoms and without sleep apnea episodes were enrolled from September 2018 to August 2019, and compared before and after surgery with thirty-four patients who had benign diseases of the thyroid or parathyroid as a control group, to investigate effects of surgery. Sleep quality was evaluated using the Japanese version of the Pittsburgh Sleep Quality Index (PSQI-J). All cases were reassessed at three months after surgery.The postoperative PSQI scores in the nasal surgery group were significantly lower than the preoperative scores (p 0.001). In contrast, there was no statistically significance difference between the pre- and postoperative PSQI scores in the neck surgery group. Difference of PSQI scores before and after surgery in the nasal surgery group was significantly higher than the neck surgery group.This double-arm study suggests that reduction of nasal disfunction with nasal surgery contributes significantly to sleep quality, in patients who may not have noticed their impaired quality of sleep previously because of their long-term nasal symptoms.

Nasal natural killer (NK)/T-cell lymphoma is a peculiar lymphoma with an unique immunophenotype. Etiologically, the authors previously first demonstrated the presence of Epstein-Barr virus (EBV) genomes and their products in this lymphoma (Lancet 1990; 335). It is suggested that some of sequence variations such as a 30-bp deletion and multiple base substitutions and as amino acid changes at HLA-A2 restricted CTL epitopes were associated with an increase in tumorigenicity and with a decrease in immune recognition. In this study, we determined full-length of LMP1 sequence isolated from 7 patients with nasal NK/T-cell lymphoma using polymerase chain reaction (PCR) method and compared the sequences with those referred to previous reports. In the carboxyl-terminal site, all 7 patients showed 4 copies of the 11 amino acids repeat (codon 254-302) and 30-bp deletion corresponding to codon 343-352 of the B95-8 strain. Within the NF-kB-activating domains, all 7 patients showed amino acid changes at codon 189 (Gln to Pro), 192 (Ser to Thr) and 212 (Gly to Ser) on either site of the PXQXT (codon 204-208) motif. In the major HLA-A2 restricted T-cell epitope sequence YLLEMLWRL (codon 125-133), all 7 patients showed amino acid changes at codon 126 (Leu to Phe) and 129 (Met to Ile). In the epitopes ALLVLYSFA (codon 51-59), VLFIFGCLL (codon 110-118) and WLLLFLAIL (codon 173-181), several patients showed novel amino acid changes at codon 59 (Ala to Gly), 110 (Val to Leu) and 174 (Leu to Ile), respectively. Although it is still not clear what the most specific and biologic variation of LMP1 gene in nasal NK/T-cell lymphoma is, the sequence data may be valuable on the study for pathogenesis of nasal NK/T-cell lymphoma and EBV molecular epidemiology.

The UL41 gene product (vhs) of herpes simplex virus (HSV) is packaged in the virion, and mediates host protein synthesis shutoff at the early stage of the virus replication cycle. In order to clarify the role of vhs in virus replication and virulence, we isolated a completely UL41-deficient mutant (the VRDelta41 strain) and its revertant (the VRDelta41R strain). In the mouse encephalitis model, the replication of strain VRDelta41 was inhibited after 2 days post-infection, resulting in low virulence, by gamma-ray-sensitive cells such as lymphocytes and/or neutrophils. The result suggested that some cytokines, produced in VRDelta41-inoculated brains, activate and induce the migration of gamma-ray-sensitive cells to the infection site. Therefore, cytokines produced by HSV-1-infected human cells were screened, and potent inductions of interleukin (IL)-1beta, IL-8 and macrophage inflammatory protein-1alpha by VRDelta41 infection were observed. Moreover, the VRDelta41 strain showed 20- and 5-fold higher sensitivity to interferon-alpha and -beta compared to the wild-type strain, respectively. These results indicate that one important role of vhs in vivo is evasion from non-specific host defence mechanisms during primary infection through suppression of cytokine production in HSV-infected cells and reduction of the anti-HSV activity of interferon-alpha and -beta.

Recurrent acyclovir (ACV)-resistant (ACV-r) herpes simplex virus type 1 (HSV-1) infections occurred in a patient with Wiskott-Aldrich syndrome, an X-linked recessive immunodeficiency syndrome composed of three clinical characteristics of immunodeficiency, thrombocytopenia, and an eczematous dermatitis. The patient had severe and recurrent ACV-r herpes simplex and was treated with vidarabine in a satisfactory manner from 1993 to 1997. During the 4-year observation period, two ACV-sensitive (ACV-s) HSV-1 isolates and five ACV-r HSV-1 isolates were recovered. The nucleotide sequence of the thymidine kinase (TK) gene from these sequential ACV-r isolates was compared with the ACV-s isolates. A single nucleotide deletion of cytosine (C) from homopolymer stretch of four C residues between nucleotide 1061 and 1064 of the open reading frame was found in all ACV-r isolates. No other differences were observed in the TK nucleotide sequence between ACV-s and ACV-r isolates. The TK nucleotide sequences of the two ACV-s isolates were identical to each other and those of the five ACV-r isolates were identical to one another. These results suggest that the ACV-r HSV-1 might have derived from the ACV-s strain in the patient body and that TK-associated ACV-r HSV-1 can reactivate from latency.

The polymorphism of the thymidine kinase (TK) gene of herpes simplex virus type 1 (HSV-1) was analyzed and was compared with the restriction fragment length polymorphism (RFLP) of the whole genome to evaluate the relative efficiency of the TK gene as a potential probe for identification and discrimination of HSV-1. The effectiveness of using the polymorphism of the TK gene in classifying HSV-1 strains was comparable to that of RFLP analysis of 66 sites, suggesting that TK gene sequencing may have important applications in epidemiological studies of HSV-1.

Nasal natural killer (NK)/T cell lymphoma is a peculiar lymphoma with a unique immunophenotype. Etiologically, in 1990, the authors first demonstrated the presence of Epstein-Barr virus (EBV) genomes and their products in this lymphoma. EBV-specific cytotoxic T lymphocytes (CTL) are very important in controlling the long-term persistence of EBV infection. Amino acid changes encoding the CTL epi-tope on the lymphoma cells may result in a reduced CTL response. We focused on two major CTL epitopes SSCSSCPLSK (codon 340 to 349) and FLYALALLLL (codon 356 to 364) of the LMP2A gene and determined the sequence isolated from nasal NK/T cell lymphoma tissues. All isolates from 7 nasal NK/T cell lymphomas showed the same amino acid change from serine to threonine at codon 348 in the CTL epitope SSCSSCPLSK. Threonine or serine substitution at codon 348 was almost equally observed in peripheral blood EBV isolates from healthy individuals in various ethnic origins. The predominant threonine substitution of nasal NK/T cell lymphoma patients may represent disease-associated polymorphism rather than a geographic or race-associated polymorphism. The LMP2A strain including threonine substitution at codon 348 may be selected within tumors and play a role for tumor genesis in Japanese patients with nasal NK/T cell lymphoma through reduced immune recognition.

A rapid phenotypic screening method for herpes simplex virus (HSV) and varicella-zoster virus (VZV) thymidine kinase (TK) genes was developed for monitoring acyclovir-resistant viruses. This method determines the biochemical phenotype of the TK polypeptide, which is synthesized in vitro from viral DNA using a procedure as follows. The TK gene of each sample virus strain is amplified and isolated under the control of a T7 promoter by PCR. The PCR products are transcribed with T7 RNA polymerase and translated in a rabbit reticulocyte lysate. Using this method, enzymatic characteristics and the size of the TK polypeptides encoding HSV and VZV DNA were defined in less than 2 days without virus isolation. The assay should be a powerful tool in monitoring drug-resistant viruses, especially in cases in which virus isolation is difficult.