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Ih-Jen Su

Publications and source records attributed to Ih-Jen Su.

At least 37 records · Page 2Linked to original sources

Laboratory-based surveillance and molecular epidemiology of influenza virus in Taiwan.

A laboratory-based surveillance network of 11 clinical virological laboratories for influenza viruses was established in Taiwan under the coordination of the Center for Disease Control and Prevention (CDC), Taiwan. From October 2000 to March 2004, 3,244 influenza viruses were isolated, including 1,969 influenza A and 1,275 influenza B viruses. The influenza infections usually occurred frequently in winter in the northern hemisphere. However, the influenza seasonality in Taiwan was not clear during the four seasons under investigation. For example, the influenza A viruses peaked during the winters of 2001, 2002, and 2003. However, some isolated peaks were also found in the summer and fall (June to November) of 2001 and 2002. An unusual peak of influenza B also occurred in the summer of 2002 (June to August). Phylogenetic analysis shows that influenza A isolates from the same year were often grouped together. However, influenza B isolates from the year 2002 clustered into different groups, and the data indicate that both B/Victoria/2/87-like and B/Yamagata/16/88-like lineages of influenza B viruses were cocirculating. Sequence comparison of epidemic strains versus vaccine strains shows that many vaccine-like Taiwanese strains were circulating at least 2 years before the vaccine strains were introduced. No clear seasonality of influenza reports in Taiwan occurred in contrast to other more continental regions.

Animals↗

Neutralizing antibody response and SARS severity.

Using the Taiwan nationwide laboratory-confirmed severe acute respiratory syndrome (SARS) database, we analyzed neutralizing antibody in relation to clinical outcomes. With a linear mixed model, neutralizing antibody titer was shown to peak between week 5 and week 8 after onset and to decline thereafter, with a half-life of 6.4 weeks. Patients with a longer illness showed a lower neutralizing antibody response than patients with a shorter illness duration (p = 0.008). When early responders were compared with most patients, who seroconverted on and after week 3 of illness, the small proportion (17.4%) of early responders (antibody detectable within 2 weeks) had a higher death rate (29.6% vs. 7.8%) (Fisher exact test, p = 0.004), had a shorter survival time of <2 weeks (Fisher exact test, p = 0.013), and were more likely to be > 60 years of age (Fisher exact test, p = 0.01). Our findings have implications for understanding the pathogenesis of SARS and for SARS vaccine research and development.

Adult↗

Evolution of pulmonary pathology in severe acute respiratory syndrome.

BACKGROUND AND PURPOSE: Severe acute respiratory syndrome (SARS) is characterized by fever with rapid progression to acute respiratory distress and it is associated with substantial morbidity and mortality. Transmission patterns suggest spread by respiratory droplet or close person-to-person contact. To elucidate the correlation of clinical presentation to the pathogenesis and course of the disease, we reviewed the pulmonary pathologic specimens of SARS patients taken at different stages of the disease. METHODS: Four "probable" cases of SARS were studied. SARS-associated coronavirus (SARS-CoV) infection was demonstrated using reverse transcriptase-polymerase chain reaction in all 4 patients. The pulmonary specimens were taken on day 7 after symptom onset in patient 1, day 11 in patient 2, day 17 in patient 3, and day 21 in patient 4. RESULTS: The autopsy lung tissue from patient 1, who died 7 days after symptoms onset due to the complication of acute myocardial infarction, revealed mild histologic change in the lung. Only focal pulmonary edema or hemorrhage was seen. In the second patient, who died 11 days after symptom onset, severe acute alveolar damage was characterized by patchy or diffuse lung edema, hyaline membrane formation, and scarce lymphocytic infiltration. The lymphocytes were mostly CD3-positive and CD20-negative. In the third patient, biopsy specimen taken 17 days after symptom onset showed patches of organizing pneumonia with reactive fibroblastic proliferation, more abundant type II pneumocytes and clustering of CD68-positive macrophages within the alveolar spaces. Few CD68-positive syncytial multinucleated giant cells were also seen in the specimens but no viral inclusion body could be identified in these cells. The lung biopsy specimen from patient 4 taken 21 days after symptom onset showed characteristics of the fibrotic stage, with significant myofibroblastic proliferation in the alveolar space and interstitium resulting in loss of pulmonary architecture. The number of CD3-positive lymphocytes and of CD68-positive macrophages in this specimen from a patient in the fibrotic phase of diffuse alveolar damage (DAD) whose condition deteriorated was less than in the specimen from case 3 who was in the early proliferative phase of DAD and eventually recovered. CONCLUSIONS: The histologic evolution of SARS coincided with the different stages of DAD: acute, proliferative organizing, and fibrotic stages. SARS cannot be differentiated from the other etiologies of DAD by morphologic examination alone. The absence of DAD does not rule out the possibility of SARS-CoV infection, particularly in the early stage of the disease.

Adult↗

Immunohistochemical study of severe acute respiratory syndrome-associated coronavirus in tissue sections of patients.

BACKGROUND AND PURPOSE: Severe acute respiratory syndrome (SARS) is a life-threatening and highly contagious disease caused by the novel SARS coronavirus (SARS-CoV). Immunohistochemical staining for SARS-CoV in the tissue sections of SARS patients is helpful in investigations of the biologic behavior of this virus in human tissue, and to determine the target cells of this virus in different organs. METHODS: We studied the pathologic specimens from 6 SARS patients by immunohistochemical staining using a specific antibody against SARS-CoV. RESULTS: Positive viral staining was only found in the lung tissue taken from the patients who died in the early stage of the disease, usually less than 10 days after symptom onset. No positive staining was found in the lung tissue specimens collected in the mid-to-late stage of the disease. The SARS-CoV-infected cells had a patchy distribution and tended to be present in the periphery of the lung. Immunohistochemically, these viral-infected cells were located mainly along the alveolar space, had a cuboidal appearance, and were reactive to cytokeratin and surfactant protein C. This suggested that type II pneumocytes are the main target cell of SARS-CoV in the lung. Occasional intra-alveolar macrophages were also weakly reactive to SARS-CoV antibody. In addition to the lung, positive viral staining was also found in the mucosal epithelium of the large intestine in another patient who had the clinical symptom of diarrhea. No evidence of viral staining was found in other organs including kidney, liver, lymph node and spleen. The skeletal muscle specimens of 2 patients who had rhabdomyolysis were also negative for SARS-CoV. CONCLUSIONS: SARS-CoV is mainly present in the cytoplasm of type II pneumocytes and can only be detected in the lung tissue during the early stage of the disease. In the patient who had symptoms of diarrhea, SARS-CoV staining was also identified in the mucosal epithelium of the colon.

Adult↗

Isolation and identification of Escherichia coli O157:H7 in a Taiwanese patient with bloody diarrhea and acute renal failure.

Escherichia coli O157:H7 is a frequent foodborne pathogen in many developed countries. Outbreaks of this infection have been reported in countries all over the world. The first clinical case of E. coli O157:H7 infection from Taiwan was reported in a 6- year-old boy who had returned from USA in August 2001. In this paper, we describe the results of the isolation and identification of this strain, and molecular typing for comparison with previously reported strains. Biochemical and molecular biological tests were used to confirm that this patient, who developed bloody diarrhea and kidney failure as a result of the infection, was indeed infected with E. coli O157:H7. None of the patients' close contacts were affected. Molecular typing by use of pulsed-field gel electrophoresis revealed this clinical strain to have a unique genotype, which is different from all available clinical strains reported from Japan and environmental strains reported from Taiwan. America Type Culture Collection reference strains and an out-break strain from USA had the nearest relationships with this clinical isolate. Molecular typing showed that this infection by E. coli O157:H7 was not derived from the local environmental strains and was acquired during overseas travel.

Acute Kidney Injury↗

Outbreak of severe acute respiratory syndrome in southern Taiwan, 2003.

This study describes the epidemiologic features of the severe acute respiratory syndrome (SARS) outbreak in southern Taiwan in 2003. According to the official files of reported cases of SARS from February 21 to June 19, 2003, there were 586 cases in southern Taiwan. Symptom onset occurred between February 21 and June 19 in reported cases, between March 13 and May 30 in probable cases, and between March 17 and May 23 in polymerase chain reaction (PCR)-positive probable cases. Dates of symptom onset were earliest for six imported cases, followed by 53 cases related to nosocomial infections and 51 cases without known sources of infection. The positive rates of the PCR for these three groups decreased from 50.0% to 28.3% to 3.9% , respectively (P < 0.001, by chi-square test for linear trend). Three other cases resulted from exposure to contaminated hospitals in northern Taiwan, one of which was the index case of the nosocomial infection. Imported cases following nosocomial infection were the major cause of SARS infections in southern Taiwan. Due to the low positive rate of the PCR for SARS coronavirus, and the low positive predictive value of reported cases, the factuality of cases with unknown sources of infection should be further verified.

Adolescent↗

Endoplasmic reticulum stress stimulates the expression of cyclooxygenase-2 through activation of NF-kappaB and pp38 mitogen-activated protein kinase.

Expression of mutant proteins or viral infection may interfere with proper protein folding activity in the endoplasmic reticulum (ER). Several pathways that maintain cellular homeostasis were activated in response to these ER disturbances. Here we investigated which of these ER stress-activated pathways induce COX-2 and potentially oncogenesis. Tunicamycin and brefeldin A, two ER stress inducers, increased the expression of COX-2 in ML-1 or MCF-7 cells. Nuclear translocation of NF-kappaB and activation of pp38 MAPK were observed during ER stress. IkappaBalpha kinase inhibitor Bay 11-7082 or IkappaBalpha kinase dominant negative mutant significantly inhibited the induction of COX-2. pp38 MAPK inhibitor SB203580 or eIF2alpha phosphorylation inhibitor 2-aminopurine attenuated the nuclear NF-kappaB DNA binding activity and COX-2 induction. Expression of mutant hepatitis B virus (HBV) large surface proteins, inducers of ER stress, enhanced the expression of COX-2 in ML-1 and HuH-7 cells. Transgenic mice showed higher expression of COX-2 protein in liver and kidney tissue expressing mutant HBV large surface protein in vivo. Similarly, increased expression of COX-2 mRNA was observed in human hepatocellular carcinoma tissue expressing mutant HBV large surface proteins. In ML-1 cells expressing mutant HBV large surface protein, anchorage-independent growth was enhanced, and the enhancement was abolished by the addition of specific COX-2 inhibitors. Thus, ER stress due either to expression of viral surface proteins or drugs can stimulate the expression of COX-2 through the NF-kappaB and pp38 kinase pathways. Our results provide important insights into cellular carcinogenesis associated with latent endoplasmic reticulum stress.

Active Transport, Cell Nucleus↗

Pre-S mutant surface antigens in chronic hepatitis B virus infection induce oxidative stress and DNA damage.

Ground glass hepatocytes (GGHs) are the historic hallmarks for the hepatocytes in the late and non-replicative stages of hepatitis B virus (HBV) infection. We have identified type I and type II GGHs that contain two mutant types of large HBV surface antigens (HBsAg) with deletions over the pre-S1 and pre-S2 regions, respectively. These pre-S mutant HBVsAg accumulate in endoplasmic reticulum (ER), resulting in strong ER stress. Type II GGHs often appear in hepatic nodules in the late phases of HBV infection and proliferate in clusters, suggesting that these mutant pre-S1/S2 HBsAg may be involved in HBV-related hepatocarcinogenesis, associated with ER stress. In this study, we investigated the potential genomic instability imposed by pre-S mutant HBsAg. Based on the analysis of comet assays, we found that the pre-S1 and pre-S2 mutant HBsAg caused oxidative stress and DNA damage. The DNA repair gene ogg1 was greatly induced by over-expression of pre-S mutant HBsAg. Induction of the DNA repair gene ogg1 was also detected in the pre-S2 HBsAg transgenic mice, as well as the type II GGHs from patients with hepatocellular carcinoma, strongly suggesting that the pre-S mutant HBsAg contributes to the oxidative DNA damage to hepatocytes. In addition, the mutation rates in the X-linked hprt gene were enhanced in mouse hepatoma ML1-4a cells, which constitutively expressed the pre-S1/S2 HBsAg. These results indicate that pre-S1/S2 mutant HBsAg, which make up GGHs, induce oxidative DNA damage and mutations in hepatocytes in the late stages of HBV infection.

Animals↗

Characterization of severe acute respiratory syndrome coronavirus genomes in Taiwan: molecular epidemiology and genome evolution.

Since early March 2003, the severe acute respiratory syndrome (SARS) coronavirus (CoV) infection has claimed 346 cases and 37 deaths in Taiwan. The epidemic occurred in two stages. The first stage caused limited familial or hospital infections and lasted from early March to mid-April. All cases had clear contact histories, primarily from Guangdong or Hong Kong. The second stage resulted in a large outbreak in a municipal hospital, and quickly spread to northern and southern Taiwan from late April to mid-June. During this stage, there were some sporadic cases with untraceable contact histories. To investigate the origin and transmission route of SARS-CoV in Taiwan's epidemic, we conducted a systematic viral lineage study by sequencing the entire viral genome from ten SARS patients. SARS-CoV viruses isolated from Taiwan were found closely related to those from Guangdong and Hong Kong. In addition, all cases from the second stage belonged to the same lineage after the municipal hospital outbreak, including the patients without an apparent contact history. Analyses of these full-length sequences showed a positive selection occurring during SARS-CoV virus evolution. The mismatch distribution indicated that SARS viral genomes did not reach equilibrium and suggested a recent introduction of the viruses into human populations. The estimated genome mutation rate was approximately 0.1 per genome, demonstrating possibly one of the lowest rates among known RNA viruses.

Base Pairing↗

Treatment outcome and pattern of failure in 77 patients with sinonasal natural killer/T-cell or T-cell lymphoma.

BACKGROUND: Sinonasal natural killer (NK)/T-cell or T-cell lymphoma behaves quite differently from other lymphomas. The objective of this study was to investigate clinical features, treatment outcomes, and failure patterns in patients with this type of sinonasal lymphoma. METHODS: From September, 1977 to December, 2000, 77 patients with sinonasal NK/T-cell lymphoma or T-cell lymphoma who had received radiotherapy (R/T), chemotherapy (C/T), or both (R/T and C/T) were evaluated retrospectively. RESULTS: Fifty-six patients (73%) had locoregional disease only, and 21 patients (27%) had systemic involvement. Forty-four patients (57%) achieved a complete remission (CR). The 5-year overall survival rate was 36% (median follow-up, 89 months). Achievement of CR was the only prognostic factor for survival in multivariate analysis. Among patients with locoregional disease, the CR rate was 63%, and the 5-year overall survival rate was 42%. Combined R/T and C/T or R/T alone resulted in better survival compared with C/T alone (5-year survival rates, 59%, 50%, and 15%, respectively; P = 0.01). Incidences of locoregional and systemic failure were 43% and 30%, respectively. Outcome was dismal for patients with systemic disease, with a CR rate of 43% and a 5-year survival rate of 25%. Only 2 of 21 patients had sustained remissions. The locoregional and systemic failure rates were 57% and 71%, respectively. CONCLUSIONS: Treatment outcomes were unsatisfactory for patients with locoregional and systemic sinonasal NK/T-cell or T-cell lymphoma. R/T could not control locoregional disease satisfactorily, and C/T was unable to eradicate systemic disease in many patients. High-dose therapy may be worth studying in these patients. New treatments should be investigated to increase remission rates, prevent failure, and improve survival.

Adolescent↗

Childhood severe acute respiratory syndrome in Taiwan and how to differentiate it from childhood influenza infection.

OBJECTIVE: To investigate clinical features and outcomes of children in Taiwan with laboratory-confirmed severe acute respiratory syndrome (SARS) vs those of children with influenza to differentiate the 2 diseases. DESIGN, SETTING, AND PARTICIPANTS: Patients 20 years or younger with clinical, epidemiological, and laboratory evidence of SARS from March to July 2003 vs children with virus culture-confirmed influenza in a 1:1 age- and sex-matched control group. MAIN OUTCOME MEASURES: Rates of symptoms, abnormal laboratory data, and outcomes of recovery, sequelae, or death. RESULTS: The 15 SARS patients (9 girls and 6 boys) had a median age of 17 years (age range, 4-20 years). Nine patients (60%) were infected through household contact, 4 (27%) nosocomially, 1 (7%) through contact with a neighbor, and 1 (7%) after returning from Hong Kong. All 15 patients had fever, 3 (20%) had chills, and 11 (73%) had cough. Only 1 patient (7%) had sputum production; 1 (7%) had rhinorrhea. At presentation, 5 patients (33%) had leukopenia, 6 (40%) had lymphopenia, and 5 (33%) had monocytopenia. All children recovered without sequelae. Children with SARS had significantly lower incidences of rhinorrhea (odds ratio [OR], 0.01; 95% confidence interval [CI], 0.00-0.09), sputum production (OR, 0.10; 95% CI, 0.02-0.63), and sore throat (OR, 0.17; 95% CI, 0.03-0.85) than children with influenza. Both groups had similar incidences of leukopenia or lymphopenia, but SARS patients had a significantly higher incidence of monocytopenia (33% vs 0%, P = .04). CONCLUSIONS: Childhood SARS is usually not fatal. The absence of rhinorrhea and presence of monocytopenia in SARS may distinguish it from influenza.

Adolescent↗

Waning immunity to plasma-derived hepatitis B vaccine and the need for boosters 15 years after neonatal vaccination.

Neonatal immunization with hepatitis B (HB) vaccine is highly effective; however, more needs to be learned about the duration of protection and indications for boosters. We measured antibody to HB core antigen (anti-HBc), HB surface antigen (HBsAg), and pre- and postbooster titers of HBsAg antibody (anti-HBs) 15 years after primary neonatal immunization with plasma-derived HB vaccines in 2 cohorts of 15-year-old children. Group A consisted of 78 children who were born to HB e antigen-positive HBsAg carrier mothers and had developed protective levels of anti-HBs antibodies (> or =10 mIU/mL) following HB immunization. Group B consisted of 113 apparently healthy children whose anti-HBs titers after vaccination were unknown. Anti-HBs was undetectable (antibody titer <10 mIU/mL) in 29.9% in group A and 62.4% in group B (P < .001). Anti-HBc was detected in 33.3 % in group A and 4.4 % in group B (P < .001). After a single booster dose of HB vaccine, 2.7% in group A and 3.3% in group B remained anti-HBs-negative. A blunted serological response was noted in approximately 20% in both groups. One HBsAg carrier was detected in group A (1.3%) and 4 in group B (3.5%). Fifteen years after neonatal immunization with plasma-derived HB vaccine, a large proportion of children exhibited waning immunity. This poses the risk of breakthrough infection. A single booster augmented the serological response to the vaccine in most but not all subjects. In conclusion, our findings suggest that one or more booster immunizations are needed in seronegative subjects by at least 15 years following neonatal immunization with plasma-derived HB vaccine.

Adolescent↗

Evaluation of antibody responses against SARS coronaviral nucleocapsid or spike proteins by immunoblotting or ELISA.

Severe acute respiratory syndrome (SARS)-CoV is a newly emerging virus that causes SARS with high mortality rate in infected people. To study the humoral responses against SARS-CoV, we evaluated nucleocapsid (N) and spike (S) proteins-specific antibodies in patients' sera by Western blotting and enzyme-linked immunosorbent assay (ELISA). Recombinant N and S proteins of SARS-CoV were purified from transformed E. coli. Serum specimens from 40 SARS-CoV-infected patients in the convalescent phase were analyzed by Western blotting using the purified antigens. Serial serum specimens from 12 RT-PCR-confirmed SARS patients were assayed by ELISA using the recombinant N protein as coated antigen. By Western blotting, 97.5% of the SARS patients were positive for N protein-specific antibodies whereas only 47.5% of the samples were positive for S protein-specific antibodies. Using N protein-based ELISA, 10 out of the 12 patients were positive for N protein-specific antibodies and 6 of them showed seroconversion at mean of 16 days after onset of fever. Immunoblotting was useful for detecting the humoral immune response after SARS-CoV infection. Antibodies against SARS-CoV N protein appear at the early stage of infection, therefore, N protein-based ELISA could serve as a simple, sensitive, and specific test for diagnosing SARS-CoV infection.

Amino Acid Sequence↗

Preparing to prevent severe acute respiratory syndrome and other respiratory infections.

Globalisation and its effect on human development has rendered an environment that is conducive for the rapid international spread of severe acute respiratory syndrome (SARS), and other new infectious diseases yet to emerge. After the unprecedented multi-country outbreak of avian influenza with human cases in the winter of 2003-2004, an influenza pandemic is a current threat. A critical review of problems and solutions encountered during the 2003-2004 SARS epidemics will serve as the basis for considering national preparedness steps that can be taken to facilitate the early detection of avian influenza, and a rapid response to an influenza pandemic should it occur.

China↗

Distribution and prognosis of WHO lymphoma subtypes in Taiwan reveals a low incidence of germinal-center derived tumors.

To assess the distribution of lymphomas in Taiwan according to the WHO (World Health Organization) classification, 175 recently diagnosed cases of malignant lymphomas were studied and the clinicopathologic data were analyzed. B-cell lymphomas accounted for 57.1% of cases, T-cell lymphomas 38.9%, and Hodgkin's lymphoma 4%. Extranodal lymphomas predominated (55.4%). The most common subtype of B-cell lymphoma was diffuse large B-cell lymphoma (33.1%). All tumor types believed to be derived from germinal center (GC) B-cells including follicular lymphoma (4.6%), Burkitt lymphoma (1.7%), Hodgkin lymphoma (4.0%), and GC-like diffuse large B-cell lymphoma (as defined by combined expression of bc1-6 and CD10) were rather uncommon as compared to frequencies seen in series from Western countries. The common T-cell lymphomas included nasal and extranasal NK/T cell lymphoma (7.4%), mycosis fungoides (7.4%), and unspecified peripheral T-cell lymphoma (6.9%). Adult T-cell leukemia/lymphoma was very uncommon and accounts for only 0.6%. The proportional increase in T-cell lymphomas that were unrelated to type I human T-cell lymphotropic virus (HTLV-1) may be linked to differential Epstein-Barr virus (EBV) oncogenesis. The survival data revealed that mantle cell lymphoma, NK/T-cell lymphoma, unspecified peripheral T-cell lymphoma, and subcutaneous panniculitis-like T-cell lymphoma had an aggressive course. Our results confirm the utility of the WHO classification scheme for prognostic stratification and further highlight the distinctive distribution pattern of malignant lymphoma in Taiwan including the higher relative incidence of T cell lymphomas and the rarity of germinal center-derived B-cell tumors.

Follow-Up Studies↗

A murine oral enterovirus 71 infection model with central nervous system involvement.

Enterovirus 71 (EV71) infection causes a myriad of diseases from mild hand-foot-and-mouth disease or herpangina to fatal meningoencephalitis complicated with neurogenic pulmonary oedema. Its pathogenesis, especially the CNS involvement, is not clearly understood. The aim of this study was to set up a mouse EV71 infection model with CNS involvement. EV71 virus was administrated orally to neonatal mice. The EV71-infected mice manifested a skin rash at an early stage and hind limb paralysis or death at a later stage. Immunohistochemical staining and virus isolation demonstrated that EV71 replicated in the small intestine, induced viraemia and spread to various organs. Kinetic studies showed that EV71 antigen was first detected in the intestine at 6 h, in the thoracic spinal cord at 24 h, in the cervical spinal cord at 50 h and in the brain stem at 78 h post-infection. Leukocyte infiltration was evident in the spinal cord and brain stem. Furthermore, EV71 virus could be transmitted to littermates within the same cage.

Administration, Oral↗

A mouse-adapted enterovirus 71 strain causes neurological disease in mice after oral infection.

A mouse-adapted enterovirus 71 (EV71) strain with increased virulence in mice, MP4, was generated after four serial passages of the parental EV71 strain 4643 in mice. Strain MP4 exhibited a larger plaque size, grew more rapidly, and was more cytotoxic in vitro than strain 4643. Although strains 4643 and MP4 both induced apoptosis of SK-N-SH human neuroblastoma cells, MP4 was more virulent than 4643 in 1-day-old mice (50% lethal doses, 10(2) and 10(4) PFU/mouse, respectively). Strain MP4 (5 x 10(6) PFU/mouse), but not 4643, could orally infect 7-day-old mice, resulting in rear-limb paralysis followed by death 5 to 9 days after inoculation with the virus. Histopathologically, neuronal loss and apoptosis were evident in the spinal cords as well as the brain stems of the infected mice. The limb muscles displayed massive necrosis. There was early and transient virus replication in the intestines, whereas the spinal cord, brain, and muscle became the sites of viral replication during the late phase of the infection. Virus transmission occurred among infected and noninfected cagemates, as demonstrated by the occurrence of seroconversion and the presence of viable viruses in the stool samples of the latter. Protection against EV71 challenge was demonstrated following administration of hyperimmune serum 1 day after inoculation with the virus. Nucleotide sequence analysis of the genome of EV71 strain MP4 revealed four nucleotide changes on the 5' untranslated region, three on the VP2 region, and eight on the 2C region, resulting in one and four amino acid substitutions in the VP2 and 2C proteins, respectively.

5' Untranslated Regions↗

Update and projection on HIV/AIDS in Taiwan.

The HIV/AIDS epidemic in Taiwan started in 1986, with 5,221 cases of HIV infections, 1,596 cases of AIDS, and 911 deaths reported through 2003. National surveillance data indicate that men who have sex with men accounted for 48.2% of HIV infections, followed by heterosexual men (33.8%) and heterosexual women (6.1%). Only 353 (6.8%) of all HIV cases are females. The average age of HIV-infected persons, AIDS cases, and deaths was 31.2, 36.2, and 39.0 years, respectively. The incidence of HIV infection has increased by approximately 15% every year since 1997. The continuing epidemic will likely burden the national health care system and may result in an estimated socioeconomic loss of U.S. dollars 1.6 billion in 2010, as 15,125 HIV infections and 1,420 deaths from AIDS are projected. To respond to the HIV/AIDS epidemic in Taiwan, the government has been working with nongovernmental organizations to promote HIV testing, conduct various education programs, and reach out to high-risk groups. HIV/AIDS patients are linked to medical care and provided with free highly active antiretroviral treatment. The main challenge is to reduce HIV-related stigma. Prevention focused on preventing further transmission of HIV by seropositive persons to others is urgently needed in fighting the HIV/AIDS epidemic.

Acquired Immunodeficiency Syndrome↗