In two consecutive studies, 80 subjects human immunodeficiency virus (HIV)-1-seropositive (21 asymptomatic, 6 persistent generalized lymphadenopathy, 13 AIDS-related complex, and 40 AIDS) were examined for oral lesions. Paired serum and saliva specimens were tested for HIV isolation, DNA, and antigen. HIV antigen was detected in sera from 31 patients, but not in saliva. HIV was isolated from blood mononuclear cells of 83% and saliva supernatants of 21%. In the second study of 25 patients, HIV was detected in plasma of 56% (titers, 1/10 to > 1/1000) but not in diluted saliva supernatants, even in those with severe periodontal disease. HIV DNA was detected using polymerase chain reaction in 2 of 7 saliva cell pellets and 4 of 5 blood samples. Hence, infectious HIV and DNA was found at very low concentrations in 21% and 28% of HIV-seropositive patients, respectively, at all stages of HIV infection.
Thrombocytopenia is a common hematologic disorder in HIV infection and occurs in both asymptomatic and AIDS patients. An autoimmune mechanism has been postulated for the platelet destruction associated with some forms of thrombocytopenia. However, recent studies revealed that megakaryocytes are susceptible to HIV infection and suggested the possibility that HIV can directly impair the platelet production from megakaryocytes. This study was designed to characterize the HIV receptor expression in megakaryocytic cells and the responsiveness to HIV infection. Four different megakaryocytic cell lines at different stages of differentiation were established from the peripheral blood of different individuals with hematologic malignancies. CMK and CMY cells (differentiated cell lines) expressed CD4, but CMS and CTS cells (poorly differentiated cell lines) did not. The HIV coreceptor CXCR4 was also expressed in CMY and CMK cells. HIV-1 (HTLV-IIIB) replicated in CMY cells persistently but not in other three cell lines. CMY cells as well as CMK cells were also susceptible to the lytic infection of HIV-2 (LAV2). Pretreatment of the CMY cells with anti-CD4 antibody inhibited the infection by both HIV-1 and HIV-2. Our results indicate that mature megakaryocytic cells express CD4 along with HIV coreceptors and are susceptible to HIV infection.
We analyzed the hemagglutinin (HA) genes of influenza A viruses consisting of 6 strains isolated from cerebrospinal fluids of patients with encephalopathy and 3 isolates from throat washes of patients without central nervous system symptoms during the 1997-1998 season in Tokyo. Aligned 9 amino acid sequences showed 7 common substitutions compared with A/Wuhan/359/95 (vaccine strain used in the season in Japan), which were allocated to three different antigenic sites on the H3 HA molecule. It is noted that a novel substitution at the receptor-binding site (Tyr-137 to Phe) was found exclusively in the isolates from the patients with encephalopathy.
Two nosocomial outbreaks of sepsis caused by Serratia marcescens, which occurred in Tokyo were the following cases. CASE A: In July 1999, 10 inpatients admitted to the third floor ward of the General Hospital A, developed sudden onset of high fever, coagulation disorders (disseminated intravascular coagulation), and acute renal failure, of which 5 died. Twenty-one strains of Serratia marcescens were isolated from the inpatient's blood and urine, nurse fingers and environmental samples from floor and cooling tower. Serratia infection was strongly suspected as the cause of sepsis. These cases were defined as "inpatients who developed fever 38 degrees C or more during July 26 to 29 and from whom S. marcescens was isolated by blood culture". Ten isolates were detected from the blood. In order to investigate the background of S. marcescens isolation in the hospital and to compare molecular and biochemical characteristics of S. marcescens, cultures were attempted from samples of other inpatients and staffs and hospital environment. Those were classified into 9 groups by various different typings: biotyping with Api Rapid 20; susceptibility typing of antimicrobial agents tested; pulsed-field gel electrophoresis (PFGE) typing of SpeI- or Xba I-restricted chromosome. All 10 isolates causing sepsis were found to be in the same group. CASE B: In January 2002, 24 inpatients, admitted to Neurosurgical Hospital B, developed sudden onset of high fever, of which 7 died. S. marcescens was isolated from a towel, environmental samples and inpatients. These cases were defined as "inpatients who developed fever of 38.5 degrees C and S. marcescens isolated by blood culture". Twelve strains were isolated from the blood samples in 12 cases. In order to investigate the background of S. marcescens isolation in the hospital, cultures were attempted from other inpatient's urine and environmental samples from medical tape, Tshake and a towel. These isolates were classified into 3 groups by the previous typings; biotyping with Api Rapid 20; susceptibility typing of antimicrobial agents tested; and PFGE typing. All 12 isolates in 12 cases were found to be in the same group. These cases of 2 nosocomial outbreaks of sepsis were defined as "in-patient who developed high fever and S. marcescens isolated by blood culture". However in both cases transmission routes of Serratia infection remain unknown by field investigation.
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