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OBJECTIVE: On 29 October 2000 poliomyelitis was officially declared to have been eradicated from the Western Pacific Region. This article describes the results of surveillance for cases of acute flaccid paralysis (AFP) in China during the final phase of the eradication effort. METHODS: We conducted hospital-based active surveillance in high-risk areas for poliomyelitis in 5 provinces of southern China (Sichuan, Yunnan, Guizhou, Guangxi and Jiangxi) between 1995 and 1997 to determine the adequacy of reporting and laboratory diagnosis of cases of AFP. FINDINGS: A total of 1069 AFP cases occurring since 1993 were identified in 311 hospital visits. Less than 50% of AFP cases occurring in 1993 and 1994 had been reported by AFP surveillance, and laboratory diagnosis had been carried out on only a small proportion of these. However, improved cooperation between hospital sectors increased the rate of case reporting and laboratory diagnosis to 85% and 78%, respectively, in 1997. Despite this overall improvement, these two indicators were approximately 10-20% lower in Yunnan Province. Epidemiological analysis revealed that cases of clinical poliomyelitis accounted for as much as one-third of all AFP in 1993 and that some of these cases were clustered. Clusters were rarely observed after 1994. Active surveillance in the China-Myanmar border areas of Yunnan over 1995-96 detected 9 cross-border cases of clinical poliomyelitis, including 2 of wild poliomyelitis. Import of poliomyelitis was thus considered to have occurred frequently until 1996 in this border area of Yunnan. These data were important for the outbreak response immunization carried out in 1996 in the border prefectures of Yunnan. CONCLUSION: Our investigation confirmed a high level of AFP surveillance in poliomyelitis high-risk areas of the five provinces and provided valuable information on the interruption of wild poliovirus circulation in southern China that will be of use to countries in other regions that have yet to eradicate poliomyelitis.

Precursor T lymphoblastic lymphoma (T-LBL) often manifests as a mediastinal mass sometimes compressing vital structures like vessels or large airways. This case was a 40-year-old male who developed T-LBL presenting as respiratory failure caused by mediastinal T-LBL. He presented with persistent life threatening hypoxia despite tracheal intubation. We successfully managed this respiratory failure using venovenous (VV) ECMO. Induction chemotherapy was started after stabilizing oxygenation and the mediastinal lesion shrank rapidly. Respiratory failure caused by compression of the central airway by tumor is an oncologic emergency. VV ECMO may be an effective way to manage this type of respiratory failure as a bridge to chemotherapy.

The human-pathogenic viruses in urban sewage have been extensively monitored to obtain information on circulating viruses in human communities. Enteroviruses (EVs) excreted by patients who present with diverse clinical syndromes can remain infectious in the environment for several weeks, and limited data on circulating environmental EVs are available. A 4-year (2009 to 2012) surveillance study was conducted to detect nonpolio enteroviruses (NPEVs) in the urban sewage of Guangzhou city, China. After the viruses in the sewage samples were concentrated and isolated, molecular identification was used to detect and type the NPEVs. During the 4-year study, 17 different NPEV serotypes were identified in the sewage of Guangzhou city. The most common serotypes were echovirus 11 (ECHO11), ECHO6, ECHO7, and ECHO12 and coxsackie group B viruses 5 (CVB5) and CVB3. The predominant serotypes were influenced by spatial and temporal factors and differed each year. CVB5 was commonly detected in 2009 and 2010 but was rarely isolated in 2011 and 2012. In contrast, CVB3 was not observed in 2009 and 2010 but was increasingly detected in 2011 and 2012. Our study provides an overview of the serotype distribution and circulation patterns of NPEVs in the sewage of Guangzhou, China. In the absence of a systematic EV disease surveillance system, the detection and characterization of sewage-borne NPEVs will help us better understand the changes in EV disease trends and the epidemic background of circulating EVs, which could help interpret the EV trends and warn of future outbreaks in this area.

Problem: On 11 March 2011, the Great East Japan Earthquake produced a catastrophic tsunami that devastated the city of Rikuzen-Takata and left it without an effective health infrastructure and at increased risk of outbreaks of disease., Approach: On 2 May 2011, a disease-surveillance team was formed of volunteers who were clinicians or members of Rikuzen-Takata's municipal government. The team's main goal was to detect the early signs of disease outbreaks., Local Setting: Seven weeks after the tsunami, 16 support teams were providing primary health care in Rikuzen-Takata but the chain of command between them was poor and 70% of the city's surviving citizens remained in evacuation centres. The communication tools that were available were generally inadequate., Relevant Changes: The surveillance team collected data from the city's clinics by using a simple reporting form that could be completed without adding greatly to the workloads of clinicians. The summary findings were reported daily to clinics. The team also collaborated with public health nurses in rebuilding communication networks. Public health nurses alerted evacuation centres to epidemics of communicable disease., Lessons Learnt: Modern health-care systems are highly vulnerable to the loss of advanced technological tools. The initiation--or re-establishment--of disease surveillance following a natural disaster can therefore prove challenging even in a developed country. Surveillance should be promptly initiated after a disaster by (i) developing a surveillance system that is tailored to the local setting, (ii) establishing a support team network, and (iii) integrating the resources that remain--or soon become--locally available.

The genetic and phenotypic characterization of poliovirus strain P3/Jinan/1/09, isolated from sewage sample in Jinan city, Shandong province, China, was described. The strain had a Sabin type 3/type 2/type 3 recombinant genome, with the first crossover site located in capsid VP1 coding region between nucleotide positions 3293 and 3294 (numbering according to Sabin 3), and the second crossover site in 3D region between positions 6374 and 6378. The recombinant had introduced six Sabin 2-derived amino acids into the carboxyl terminus of Sabin 3 VP1 capsid protein. The complete genome of the isolate revealed eight nucleotide substitutions in Sabin 3 region with two substitutions resulting in amino acid alteration, and two missense substitutions in the Sabin 2 region. An estimation based on the evolution rate of the P1 coding region of Sabin 3 background suggested that evolution time of strain P3/Jinan/1/09 might be 76-80 days. The person who excreted the recombinant was not known and no evidence was obtained for its circulation in population via acute flaccid paralysis surveillance. The virus showed Sabin 3 serological characterization in neutralization test, and it did not lose temperature sensitivity phenotype at 40 degrees C. The significance of environmental surveillance and the presence of natural capsid recombinant poliovirus strain in the context of the global polio eradication initiative are discussed., ((c) 2010 Elsevier B.V. All rights reserved.)

We successfully isolated Cryptococcus neoformans from chicken faeces in suburban areas of Thailand. C. neoformans was isolated from 36/150 houses (24.0%) in the dry season and 6/150 (4.0%) in the rainy season. All environmental isolates were of serotype A. The high isolation rate of 24% from chicken faeces has never been reported previously. Our environmental study could probably explain the high incidence of cryptococcal meningitis in HIV patients in Thailand.

Approximately 1% (4/500) of blood donors exhibited seropositivity for HTLV-II in South Vietnam, but none (0/500) did in North Vietnam. Further, all individuals seropositive for HTLV-II were intravenous drug abusers who were seronegative for HIV-1 and HTLV-I. These findings suggest that HTLV-II infection may be specifically prevalent in drug abusers in South Vietnam.

Blood donors in two cities in Vietnam were tested for markers of hepatitis C virus (HCV) and hepatitis B virus infections. Antibody to HCV was detected by passive hemagglutination with antigens of the second generation in 101 (20.6%) of 491 donors in Ho Chi Minh City; it was detected less frequently (P < 0.001) in donors in hanoi (4 [0.8%] of 499). HCV RNA was tested for in donors with antibody by PCR with nested primers from the 5'-noncoding region and detected in 79 donors in Ho Chi Minh City and 4 donors in Hanoi. HCV RNA was genotyped by PCR with type-specific primers from the core gene. Of 83 HCV carriers from Vietnam, 24 (29%) were infected with HCV of genotype I/1a 19 (23%) were infected with II/1b, 4 (5%) were infected with III/2a, and 2 (2%) were infected with mixed genotypes (I/1a and II/1b); HCV genotypes in the remaining 34 (41%) donors, including all 4 donors in Hanoi, were not classifiable into I/1a, II/2a, IV/2b, or V/3a. Of the 10 isolates with unclassifiable genotypes, 2 showed substantial sequence divergence within the 5'-noncoding region from reported isolates with known genotypes (I/1a to 6a). An analysis of part of the core gene sequence indicated that six of the remaining isolates most likely represented new HCV genotypes. Hepatitis B surface antigen and the corresponding antibody, respectively, were detected in 15 (3.1%) and 234 (47.7%) donors in Ho Chi Minh City as well as 15 (3.0%) and 248 (49.7%) donors in Hanoi. These results indicate an extensive spread of HCV among Ho Chi Minh City donors and HCV of novel genotypes in vietnam.

Adult T-cell leukemia virus (ATLV)-associated antigen was induced in normal human peripheral or cord lymphocytes by inoculation of cell-free ATLV from a producer line, MT-2. Induction of the antigen was much more efficient, when the cells were treated with phytohemagglutinin before infection. Most ATLV-specific antigen (ATLA)-positive cells induced by ATLV in peripheral lymphocytes formed rosettes with sheep erythrocytes, but 20 to 40% of those induced in cord lymphocytes were not rosette-forming cells. Continuous proliferation of ATLA-positive cells was not observed.

Sera from 154 hemophiliacs, including 132 with hemophilia A and 22 with hemophilia B, were examined for antibodies against human T cell lymphotropic virus type III (HTLV-III) and type I by strip radioimmunoassay based on the Western blotting technique. Sixty-two patients lived in Kyushu, a known endemic area of HTLV-I and 92 patients lived in Tokyo, a nonendemic area of HTLV-I. Results showed a prevalence of HTLV-III antibodies of 64.5% in Kyushu and of 57.6% in Tokyo. There were no significant differences between these two groups. Helper/suppressor (T4/T8) ratios of seropositive patients were 0.69 +/- 0.41 and those of seronegative patients were 1.05 +/- 0.56. Ratios of both groups were lower than those of normal healthy people (1.35 +/- 0.45). Our findings confirmed that hemophiliacs living in an HTLV-I endemic area and those living in a nonendemic area in Japan equally possessed antibodies to HTLV-III. Low T4/T8 ratios and increases of serum IgG and IgM levels were found even in seronegative hemophiliacs.

Antibodies against human T-cell lymphotropic virus type I (HTLV-I) in the sera from 60 patients with adult T-cell leukemia and 21 carriers who were suspected of having HTLV-I infection were investigated by indirect immunofluorescence assay (IFA), enzyme-linked immunosorbent assay (ELISA), membrane immunofluorescence assay (MIA) and strip radio immunoassay based on the western blotting technique (SRIA). The sera of 2 of the carriers who were seropositive in IFA and ELISA were negative in MIA and did not react with virus-specific proteins by SRIA. Two sera were negative in IFA and ELISA. These sera were positive in MIA and reacted with only the envelope-related glycoprotein (gp46) and not with gag-related proteins (p28, p24, p19) by SRIA. These findings suggest that the main antigens defined by IFA and ELISA are gag-related proteins and some sera which do not contain anti-HTLV-I antibodies give false-positive results because of the reaction to unknown cellular components. Also some sera may have antibodies against only envelope glycoproteins, and these sera may give false-negative results in IFA and ELISA.

Mouse monoclonal antibodies, GIN-2, -7 and -14, against adult T-cell leukemia virus (ATLV) were prepared by a hybridoma procedure. These antibodies belonged to different subclasses of IgG, but they reacted similarly with both ATLV-specific polypeptides p19 and p28. In the reaction with monoclonal antibodies and various ATLV-producer cell lines, it was found that MT-2 and MT-2-related T-cell lines produced both p19 and p28, whereas MT-2-unrelated cell lines produced p19, but not p28.

A newly found human retrovirus, adult T-cell leukemia virus (ATLV) was shown by means of membrane immunofluorescence to bind to various hematopoietic cells including T-, B- and non-T, non-B-cell lines. Partially purified viral gp46 from culture fluids of ATL virus producer lines also bound efficiently to an ATLV-negative T-cell line, CCRF-CEM cells. When the viruses were pre-incubated with anti-ATLV-positive human sera, ATLV binding to the cells was clearly inhibited but not by pre-incubation with anti-ATLV-negative sera. These data suggest that: (1) ATLV binds not only to T-cells but also to multiple types of cells of hematopoietic origin; (2) anti-ATLV antibody-positive human sera have the blocking antibody for the binding of ATLV to lymphoid cells.

Adult T-cell leukemia-associated membrane antigen (ATLMA) expressed on the surface of living ATL virus (ATLV)-carrying cells was investigated by an indirect membrane immunofluorescence method using natural antibodies to ATLV in human sera. All the ATLV-positive cell lines tested that had cytoplasmic ATL-associated antigen (ATLA) detectable in acetone-fixed cell smears were also positive for ATLMA, but ATLMA was not detected in any ATLV-negative cell lines. The frequencies of ATLA- and ATLMA-bearing cells in seven cell lines tested were roughly parallel. The frequency of expression of both ATLMA and ATLA in cultures of MT-1 cells increased in the presence of 5-iodo-2'-deoxyuridine. All human sera having ATLA antibody had ATLMA antibody and the titers of the two were similar in most of the sera. The anti-ATLMA titers of human sera determined by using an ATLV-bound non-ATL T-cell line as antigen were also similar to the anti-ATLA titers. Absorption of anti-ATLMA-positive sera with living MT-2 cells, in which almost 100% of the cells express ATLA and ATLMA, caused parallel decreases in the anti-ATLA and anti-ATLMA titers. Analysis of the 125I-labeled surface of MT-2 cells by immunoprecipitation with anti-ATLMA-positive human serum followed by gel electrophoresis revealed that p19, p24, p28, and p46 polypeptides were specifically precipitated. These data suggest that ATLMA on the cell surface is not distinguishable from ATLA in the cytoplasm.

Eight lymphoblastoid cell lines were established from the peripheral blood of individual African green monkeys (AGM). The AGM-2206 line grew out spontaneously. The others - AGM-6, 7, 8, 10, 12, 13, and 16 - were obtained after infection of peripheral AGM lymphocytes with cell-free culture supernatant of AGM-2206. All lines contained, and were probably transformed by, AGM-EBV. Moreover, they expressed immunoglobulins but lacked the Leu l T-cell marker. Thus they were B cells. Since a high percentage of AGMs are naturally infected with a virus similar to adult T-cell leukemia virus (ATLV), we examined these cell lines for ATLV. With immunofluorescence tests we detected ATLV-related antigens (ATLA) in three of the eight cell lines. EBV membrane antigen was present in three out of four. The highest percentage (40%) of ATLA-positive cells was found in the AGM-13 line. After metabolic labelling of these cells, ATLV-specific polypeptides p24, p19, p15, and p10 were detected. Hybridization experiments showed that both AGM-2206 and AGM-13 cell lines contained ATLV-proviral DNA. Electron micrographs of AGM-13 revealed a few type-C particles morphologically similar to the MT-2 virus. By cocultivation this AGM virus was able to infect and immortalize human peripheral blood lymphocytes. One such human cell line, NA-13, expressed polypeptides closely related to ATLV core antigens but a 68,000 mol.wt. glycopolypeptide was serologically distinct from MT-2 ATLV gp68.

We have examined expression of antigens defined by HT462 monoclonal antibody (mAb), together with other HTLV-I related antigens using phorbol 12-myristate 13-acetate treated leukemic mature T cells. Thirteen patients with adult T-cell leukemia (ATL), 3 patients in remission states of ATL and 5 patients with non-ATL were examined. All ATL cells expressed the HT462 antigen, however cells from patients in remission did not express the HT462 antigen. A low percentage of cells from 2 out of 5 patients with non-ATL mature leukemic T cells expressed the HT462 antigen, although these cells did not express other HTLV-I related antigens. Cells of HTLV-I infected human cell lines expressed the HT462 antigen. Three HTLV-I infected rat cell lines (TARS-1, TART-1, TARL-2) did not express the HT462 antigen, although cells of these lines expressed other HTLV-I related antigens. Characterization of the HT462 antigen by strip radioimmunoassay based on western blotting technique using cell lysates of HUT102 cells revealed two additional bands (p68, p35) together with previously reported proteins (gp52, p42). Only p68 was seen in western blots using cell lysates of the rat cell lines. These findings further suggest that the HT462 antigen is a cellular component induced in virus transformed human cells and not a virus encoded protein.