Chikungunya fever (CHIK) is an acute viral infection caused by infection with chikungunya virus (CHIKV). The disease affects people in areas where certain Aedes species mosquito vectors are present, especially in tropical and subtropical countries. Indonesia has witnessed CHIK disease since the early 1970s with sporadic outbreaks occurring throughout the year. The CHIK clinical manifestation, characterized by fever, headache, and joint pain, is similar to that of dengue (DEN) disease. During a molecular study of a DEN outbreak in Jambi, Sumatra, in early 2015, DENV-negative samples were evaluated for evidence of CHIKV infection. Among 103 DENV-negative samples, eight samples were confirmed (7.8%) as positive for CHIKV by both molecular detection and virus isolation. The mean age of the CHIK patients was 21.3 ± 9.1 (range 11–35 years). The clinical manifestations of the CHIK patients were mild and mimicked DEN, with fever and headache as the main symptoms. Only three out of eight patients presented with classical joint pain. Sequencing of the envelope glycoprotein E1 gene and phylogenetic analysis identified all CHIKV isolates as belonging to the Asian genotype. Overall, our study confirms sustained endemic CHIKV transmission and the presence of multiple arboviruses circulating during a DEN outbreak in Indonesia. The co-circulation of arboviruses poses a public health threat and is likely to cause misdiagnosis and underreporting of CHIK in DEN-endemic areas such as Indonesia.

: Chikungunya virus (CHIKV) is recognized but rarely considered as a cause of central nervous system infection in endemic areas. A total of 244 patients with acute meningoencephalitis in Indonesia were retrospectively tested to identify whether any CHIKV infection was associated with neurological manifestations, especially in provinces known for CHIKV endemicity. Cerebrospinal fluid (CSF) and blood specimens were tested using CHIKV-specific real-time reverse transcription polymerase chain reaction and IgM ELISA, alongside a panel of neurotropic viruses. We report four cases of suspected or confirmed CHIKV-associated neurological disease, including CHIKV RNA detection in CSF of one patient and in acute serum of another, and CHIKV IgM in CSF of three patients and in serum of a fourth. In conclusion, CHIKV should be considered as a cause of neurologic disease in endemic areas and especially during outbreaks, in addition to the more common arboviral diseases such as dengue and Japanese encephalitis viruses.

Dengue is a mosquito-borne disease of public health concern affecting tropical and subtropical countries, including Indonesia. Although studies on dengue epidemiology have been undertaken in Indonesia, data are lacking in many areas of the country. The aim of this study was to determine dengue virus (DENV) and chikungunya virus (CHIKV) molecular epidemiology in western regions of the Indonesian archipelago. A one-year prospective study was conducted in Aceh and Jambi in 2015 and 2016, respectively, where patients with dengue-like illness were enrolled. Of 205 patients recruited, 29 and 27 were confirmed with dengue in Aceh and Jambi, respectively, and three from Jambi were confirmed with chikungunya. DENV-1 was the predominant serotype identified in Aceh while DENV-2 was predominant in Jambi. All DENV-1 and DENV-2 from both regions were classified as Genotype I and Cosmopolitan genotype, respectively, and all DENV-3 viruses from Jambi were Genotype I. Some viruses, in particular DENV-1, displayed a distinct lineage distribution, where two DENV-1 lineages from Aceh were more closely related to viruses from China instead of Jambi highlighting the role of travel and flight patterns on DENV transmission in the region. DENV-2 from both Aceh and Jambi and DENV-3 from Jambi were all closely related to Indonesian local strains. All three CHIKV belonged to Asian genotype and clustered closely with Indonesian CHIKV strains including those previously circulating in Jambi in 2015, confirming continuous and sustainable transmission of CHIKV in the region. The study results emphasize the importance of continuous epidemiological surveillance of arboviruses in Indonesia and simultaneous testing for CHIKV among dengue-suspected patients.

Chikungunya fever is a self-limiting viral illness that is caused by the chikungunya virus (CHIKV). CHIKV is found in multiple provinces of Indonesia, with clustered local outbreaks. This case series investigates a local chikungunya outbreak during the COVID-19 pandemic, involving two virologically confirmed chikungunya cases found in Jambi, Sumatra, Indonesia in 2021 and the contact tracing of 65 people from the same neighborhood (one of which was also virologically confirmed with CHIKV). The two original cases were symptomatic with classic signs of chikungunya fever, while the CHIKV-positive neighbor was asymptomatic. Out of the 65 participants, chikungunya IgM was detected in seven (10.8%) people while chikungunya IgG was detected in six (9.2%) using capture ELISA. Dengue IgG was detected by rapid test in three (4.6%) of the participants, showcasing a history of dengue virus (DENV) infection along with the circulation of CHIKV in the area. A phylogenetic analysis demonstrates a close evolutionary relationship between all three 2021 Jambi CHIKV isolates and the 2015–2016 isolates from Jambi. This case series showcases the endemicity and persistent circulation of CHIKV in Jambi, leaving the area vulnerable to eminent outbreaks of chikungunya fever and doubling the burden of disease during the COVID-19 pandemic. Health staff training for case detection and notification, as well as an integrated vector surveillance should continue to be implemented to provide an early warning indicator of possible chikungunya outbreaks.

Introduction: Sepsis mortality rate in Indonesia reaches over 50 %, hence, acknowledgement of its pathophysiology need to be elucidated, including the pathway of apoptotic. The objective of this study was to describe the lipopolysaccharide (LPS)-induced sepsis in which triggers intrinsic apoptotic pathways in terms of the expression of caspase-9 (Cas9) and caspase-3 (Cas3). Method: By experimental with time series randomized post test-only control group design, 48 Balb/C mice divided into 2 groups (control and treatment). Each group was injected intra-peritoneally with saline 250 µL/mice and saline 250 µL + 0.1 mg E. coli LPS/mice. Each group divided into 4 termination time (12^th, 24^th, 36^th and 48^th hours), examined by immunohistochemistry (IHC) for Cas9 and Cas3 expression, and analyzed by mean difference test (Mann-Whitney and t test) and correlation test (Spearman’s test). Results: The LPS-induced sepsis in the treatment group revealed increasing number of caspase-9 compared to control group (2.34+0.24 vs 0.82+0.08; p<0.001. There were increasing trends in the treatment group compared to control group includes for: all groups Cas3 (1.54+0.10 vs 0.48+0.05; p<0.001), t12 Cas3 (3.25+0.22 vs 0.50+0.06; p<0.001), t24 Cas3 (1.37+0.27 vs 0.45+0.05; p=0,002), and t36 Cas3 (1.03+0.20 vs 0.52+0.22; p=0,002). Instead, there were no difference between treatment group and control group for t48 Cas3 (0.50+0.14 vs 0.43+0.10; p=0,485). There was decreasing pattern on serial time 12, 24, 36 and 48 hours for Cas9 (p<0,001) and Cas3 (p=0,002). There was a correlation between Cas9-Cas3 (r_s=0.835;p=0.001). Conclusion: The LPS-induced sepsis caused an increase of caspase-9 and caspase-3, strongly correlated with decreasing pattern on time serial.

Sepsis remains a health problem because of the high related mortality and morbidity. One of the efforts is the improvement of knowledgeabout manifestation and pathophysiology of sepsis at the level of molecular biology. Nitric oxide (NO) levels increased in sepsis and this isrelated to the occurrence of cell apoptosis. The purpose of this study was to know and to see the clinical picture of sepsis and elevated levels ofNO in mice Balb/C which were injected with lipopolysaccharide (LPS). In this research, the mice were divided into three (3) groups, groupA were injected with saline, group B were injected with LPS 0.1 mg per mouse, while group C was injected with 0.2 mg per mouse. Themice were then measured by clinical parameters from day 0 and day 1, and 3,5 to 7. The levels of NO were assessed by blood sampling asmuch as 1 cc from the peri orbital plexus and examined by Griess method on days 1, 3, 5, 7. The results of the study showed that from theweight parameter there was a decrease in body weight on day 1 in group B and C and the weight continued to decline until day 3. From thetemperature parameter it was shown that the temperature decreased both in group B and C on day 1 but on day 3 and so on varies in bothgroups. From the piloerection parameters from day 1 to day 7 showed that there was piloerection in both groups. Related to the discharge byperi orbital parameters and diarrhoea many variations, occurred on day 1 peri orbital discharge and diarrhoea was found, but not uniformlyin all the mice in each group. On day 5 and 7 the peri orbital discharge and diarrhoea were not visible. NO levels increased mainly on day3 and the percentage was higher in group C and on day 5 and day 7 the levels were negative. In conclusion in this study it was shown, thatthe clinical picture is striking, weight loss and increased levels of NO occurs on day 3 of the observation.