Background Transmission within families and multiple spike protein mutations have been associated with the rapid transmission of SARS-CoV-2. We aimed to: (1) describe full genome characterization of SARS-CoV-2 and correlate the sequences with epidemiological data within family clusters, and (2) conduct phylogenetic analysis of all samples from Yogyakarta and Central Java, Indonesia and other countries. Methods The study involved 17 patients with COVID-19, including two family clusters. We determined the full-genome sequences of SARS-CoV-2 using the Illumina MiSeq next-generation sequencer. Phylogenetic analysis was performed using a dataset of 142 full-genomes of SARS-CoV-2 from different regions. Results Ninety-four SNPs were detected throughout the open reading frame (ORF) of SARS-CoV-2 samples with 58% (54/94) of the nucleic acid changes resulting in amino acid mutations. About 94% (16/17) of the virus samples showed D614G on spike protein and 56% of these (9/16) showed other various amino acid mutations on this protein, including L5F, V83L, V213A, W258R, Q677H, and N811I. The virus samples from family cluster-1 (n = 3) belong to the same clade GH, in which two were collected from deceased patients, and the other from the survived patient. All samples from this family cluster revealed a combination of spike protein mutations of D614G and V213A. Virus samples from family cluster-2 (n = 3) also belonged to the clade GH and showed other spike protein mutations of L5F alongside the D614G mutation. Conclusions Our study is the first comprehensive report associating the full-genome sequences of SARS-CoV-2 with the epidemiological data within family clusters. Phylogenetic analysis revealed that the three viruses from family cluster-1 formed a monophyletic group, whereas viruses from family cluster-2 formed a polyphyletic group indicating there is the possibility of different sources of infection. This study highlights how the same spike protein mutations among members of the same family might show different disease outcomes.

Background Severe acute respiratory infection (SARI) accounts for a large burden of illness in Indonesia. However, epidemiology of SARI in tertiary hospitals in Indonesia is unknown. This study sought to assess the burden, clinical characteristics, and etiologies of SARI and concordance of clinical diagnosis with confirmed etiology. Methods Data and samples were collected from subjects presenting with SARI as part of the acute febrile Illness requiring hospitalization study (AFIRE). In tertiary hospitals, clinical diagnosis was ascertained from chart review. Samples were analyzed to determine the “true” etiology of SARI at hospitals and Indonesia Research Partnership on Infectious Diseases (INA‐RESPOND) laboratory. Distribution and characteristics of SARI by true etiology and accuracy of clinical diagnosis were assessed. Results Four hundred and twenty of 1464 AFIRE subjects presented with SARI; etiology was identified in 242 (57.6%), including 121 (28.8%) viruses and bacteria associated with systemic infections, 70 (16.7%) respiratory bacteria and viruses other than influenza virus, and 51 (12.1%) influenza virus cases. None of these influenza patients were accurately diagnosed as having influenza during hospitalization. Conclusions Influenza was misdiagnosed among all patients presenting with SARI to Indonesian tertiary hospitals in the AFIRE study. Diagnostic approaches and empiric management should be guided by known epidemiology. Public health strategies to address the high burden of influenza should include broad implementation of SARI screening, vaccination programs, clinician education and awareness campaigns, improved diagnostic capacity, and support for effective point‐of‐care tests.

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Table of contentsA1 Hope and despair in the current treatment of nasopharyngeal cancerIB TanI1 NPC international incidence and risk factorsEllen T ChangI2 Familial nasopharyngeal carcinoma and the use of biomarkersChien-Jen Chen, Wan-Lun Hsu, Yin-Chu ChienI3 Genetic susceptibility risk factors for sporadic and familial NPC: recent findingsAllan HildesheimI5 Genetic and environmental risk factors for nasopharyngeal cancer in Southeast AsiaJames D McKay, Valerie Gaborieau, Mohamed Arifin Bin Kaderi, Dewajani Purnomosari, Catherine Voegele, Florence LeCalvez-Kelm, Graham Byrnes, Paul Brennan, Beena DeviI6 Characterization of the NPC methylome identifies aberrant epigenetic disruption of key signaling pathways and EBV-induced gene methylationLi L, Zhang Y, Fan Y, Sun K, Du Z, Sun H, Chan AT, Tsao SW, Zeng YX, Tao QI7 Tumor exosomes and translational research in NPCPierre Busson, Claire Lhuillier, Olivier Morales, Dhafer Mrizak, Aurore Gelin, Nikiforos Kapetanakis, Nadira DelhemI8 Host manipulations of the Epstein-Barr virus EBNA1 proteinSheila Mansouri, Jennifer Cao, Anup Vaidya, and Lori FrappierI9 Somatic genetic changes in EBV-associated nasopharyngeal carcinomaLo Kwok WaiI10 Preliminary screening results for nasopharyngeal carcinoma with ELISA-based EBV antibodies in Southern ChinaSui-Hong Chen, Jin-lin Du, Ming-Fang Ji, Qi-Hong Huang, Qing Liu, Su-Mei CaoI11 EBV array platform to screen for EBV antibodies associated with NPC and other EBV-associated disordersDenise L. Doolan, Anna Coghill, Jason Mulvenna, Carla Proietti, Lea Lekieffre, Jeffrey Bethony, and Allan HildesheimI12 The nasopharyngeal carcinoma awareness program in IndonesiaRenske Fles, Sagung Rai Indrasari, Camelia Herdini, Santi Martini, Atoillah Isfandiari, Achmad Rhomdoni, Marlinda Adham, Ika Mayangsari, Erik van Werkhoven, Maarten Wildeman, Bambang Hariwiyanto, Bambang Hermani, Widodo Ario Kentjono, Sofia Mubarika Haryana, Marjanka Schmidt, IB TanI13 Current advances and future direction in nasopharyngeal cancer managementBrian O’SullivanI14 Management of juvenile nasopharyngeal cancerEnis OzyarI15 Global pattern of nasopharyngeal cancer: correlation of outcome with access to radiotherapyAnne WM LeeI16 The predictive/prognostic biomarker for nasopharyngeal carcinomaMu-Sheng ZengI17 Effect of HLA and KIR polymorphism on NPC riskXiaojiang Gao, Minzhong Tang, Pat Martin, Yi Zeng, Mary CarringtonI18 Exploring the Association between Potentially Neutralizing Antibodies against EBV Infection and Nasopharyngeal CarcinomaAnna E Coghill, Wei Bu, Hanh Nguyen, Wan-Lun Hsu, Kelly J Yu, Pei-Jen Lou, Cheng-Ping Wang, Chien-Jen Chen, Allan Hildesheim, Jeffrey I CohenI19 Advances in MR imaging in NPCAnn D KingO1 Epstein-Barr virus seromarkers and risk of nasopharyngeal carcinoma: the gene-environment interaction study on nasopharyngeal carcinoma in TaiwanYin-Chu Chien, Wan-Lun Hsu, Kelly J Yu, Tseng-Cheng Chen, Ching-Yuan Lin, Yung-An Tsou, Yi-Shing Leu, Li-Jen Laio, Yen-Liang Chang, Cheng-Ping Wang, Chun-Hun Hua, Ming-Shiang Wu, Chu-Hsing Kate Hsiao, Jehn-Chuan ...

Background Rubella infection in pregnancy can cause congenital rubella syndrome (CRS), and one common defect of CRS is hearing loss. However, hearing screening is not routinely performed in Indonesia. While the number of reported cases of CRS in Indonesia is increasing, it is still difficult to identify all CRS cases. This study aims to identify CRS cases through a newborn hearing screening. Materials and Methods This descriptive study was conducted at Dr. Sardjito Hospital, Yogyakarta, Indonesia. The subjects were recruited from September 1, 2013 to November 19, 2013. The study period was from September 1, 2013 to January 31, 2014. Newborn subjects underwent the first otoacoustic emissions (OAEs) test. Subjects with the first OAEs test REFER results underwent the second OAEs test 2 months later. Subjects with REFER result in the second OAEs test then underwent auditory brainstem response (ABR) and detection of rubella IgM in blood serum. Result There were 151 subjects who underwent the first OAEs test. Ninety subjects (60%) had REFER results, but only 29 subjects underwent the second OAEs test. In the second OAEs test, 9/151 (5%) subjects were REFER. There were 6/151 (3.9%) subjects who underwent ABR and all subjects had sensory neural hearing loss. Of them, one subject was positive for rubella IgM with a titer of 11.86 at 2.5 months of age. We found nine suspected CRS cases, one clinically-confirmed and one laboratory-confirmed CRS case. The incidence of laboratory-confirmed CRS was 1/151 (6.62/1,000) live births. Conclusion Due to the low incidence we found and the cost of screening, we recommend to strengthen surveillance of CRS. All infants less than 1 year of age with suspected CRS should be checked with rubella IgM to identify CRS cases. While universal newborn hearing screening is not mandatory in Indonesia, targeted newborn hearing screening should be performed to detect children with permanent congenital hearing loss due to CRS.

Cellular immunity plays an important role in viral infection. The activation of effector T-lymphocytes and the release of cytokines define the course of dengue viral infection. CD4+ T-lymphocyte induces the immunopathology via various mechanisms; however, its kinetics in different onset of fever and disease severity are not fully understood. This study was conducted to observe the kinetics of CD4 + T-lymphocyte level among dengue infected patients and to obtain the absolute cell count and relative percentage of CD4 + T-lymphocyte. This was a descriptive study on thirty six patients who met the WHO-1997 criteria of dengue infection, hospitalized in Dr. Sardjito Hospital in the period of March to May 2009. The CD4 + T-lymphocytes were examined using the flow cytometer. The significance of median CD4 + T-lymphocytes among days were assessed using Kruskal-Wallis and Mann-Whitney SPSS 11 for Window. The absolute CD4 + T-lymphocyte was significantly different among days (p<0.05) between DF and DHF patients, while the relative CD4 + percentage count was not different (p>0.05). The absolute CD4 + T-lymphocytes count was low in the beginning of the disease course and increased from the 2nd day of fever to the normal level on the 7th day. In conclusion, DF and DHF do not differ in the absolute CD4 + T-lymphocytes count as well as in the relative CD4+ T-lymphocytes percentage. [MKB. 2014;46(4)

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Systemic Lupus Erythematosus (SLE) is an autoimmune disease that affects various body organs and causes chronic inflammation. Thrombocytopenia is common in SLE, and there is a risk of causing bleeding, which can result in death. This study aimed to analyze the relationship of thrombocytopenia with bleeding and poor clinical outcomes in SLE patients at Dr. Sardjito Hospital. The design of this study was retrospective observational analytic. The research subjects were patients diagnosed with SLE at Dr. Sardjito Hospital from January 2016-December 2019 who conducted ANA and anti-dsDNA examinations. Statistical analysis using MedCalc version 13.0. Receiver operating characteristic curve analysis to determine the cut-off value of the platelet count for the occurrence of bleeding. Chi-Square for trend test to determine the relationship between the degree of thrombocytopenia and the degree of bleeding. Kaplan-Meier test to determine the six months survival analysis for SLE patients. There were 61 SLE patients at Dr. Sardjito Hospital. Thirty-two patients (52.5%) had thrombocytopenia. The AUC of the platelet count for the occurrence of hemorrhage was 0.988 (95% CI=0.918-1, p < 0.0001), the cut-off value was 146x103/L, sensitivity 100%, specificity 90.6%, and LR+ 10.33. The AUC of the platelet count for grade 3 hemorrhage was 0.929 (95% CI=0.833-0.979, p < 0.0001), cut-off value 91x103/L, sensitivity 100%, specificity 89.3%, and LR+ 9.33. Hemorrhage was seen in 29 subjects with thrombocytopenia. Five subjects (8.2%) died, with a significant difference in the mortality of SLE patients with and without thrombocytopenia in the six months survival analysis (p=0.028). The risk of hemorrhage and poor clinical outcome (death) were significantly higher in SLE patients with thrombocytopenia and increased with the thrombocytopenia grade.