Summary. -The dengue disease varies clinically from mild fever to hemorrhagic fever up to potentially fatal shock syndrome. Such differences in manifestation of dengue virus (DENV) infection have been ascribed to intrinsic differences in DENVs. Four DENV serotypes or four dengue viruses (DENV-1 to DENV-4) have been clearly distinguished; however, only limited information is available on their biological characteristics in vitro. To shed more light on this subject, replication kinetics of all four DENVs in various cell lines and induction of 26 cytokines/chemokines were investigated. The results showed that, (i) all DENVs replicated relatively similarly in various cell lines, (ii) DENV-1 was most effective in this regard, (iii) A549 cells showed the highest virus replication rate compared to other cells, and (iv) all DENVs induced in A549 cells similar levels of several cytokines/chemokines, namely eotaxin, granulocyte colony stimulating factor (G-CSF), interferon alpha 2 (IFN-α2), interleukins 6, 8 15 (IL-6, IL-8, IL-15), and IP-10. In conclusion, this study revealed a similarity in growth characteristics and cytokine/chemokine induction profile for all four DENV serotypes in vitro.

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Background: Efforts in reproductive preservation for cancer patients have become one of the important aspects of cancer management. In fact, decline in reproductive function is known to occur after exposure to anti-cancer treatments. Measuring anti-Müllerian hormone (AMH) levels is known to be the best parameter in predicting ovarian reserves, which indicates reproductive function. In total, 68% of cancer survivors of reproductive age who underwent anti-cancer treatments suffer from infertility. Meanwhile, ovarian reserves also decrease with increasing age. There is ongoing debate on whether the ovarian reserves of cancer patients could be reduced long before exposure to anti-cancer therapy. Therefore, it is important to know whether ovarian reserves in cancer patients decrease before or after anti-cancer therapy. This can help predict the reproductive function in such cases and the effectiveness of ovarian preservation efforts. Methods: A cross-sectional study was conducted, comparing the AMH levels of 44 female cancer patients of reproductive age before cancer therapy, to 44 non-cancer patients of reproductive age (age matched). The biological ages from both groups were adjusted using the Indonesian Kalkulator of Oocytes. Results: The median age in both groups was 28 years old. The AMH levels in the cancer group were found to be significantly lower in contrast to those in the non-cancer group (1.11 [0.08-4.65] ng/ml vs. 3.99 [1.19- 8.7]; p- value <0.001). Therefore, the biological age in the cancer group was 10 years older than that of the non-cancer group, indicating that ovarian aging occurs earlier in cancer patients. Conclusions: AMH levels of cancer patients of reproductive age were already reduced before cancer therapy, given an older biological age, in contrast to that of the non-cancer patients. Proper counseling and implementation of fertility-preserving methods is highly recommended in this group of patients.

Background: Recently, as a delayed childbearing trend is emerging in modern women’s adulthood, diminished reproductive potential due to age-related changes is more prevalent. Reduction in the abundance of mitochondrial DNA (mtDNA) copies and circulating anti-Müllerian hormone (AMH) have been separately reported with aging, contributing to the decrease in successful reproduction. However, there are limited reports on the impact of age on mtDNA and AMH in the same individual and whether mtDNA copy numbers are influenced by age and AMH. Methods: In the present study, we utilized a real-time quantitative PCR (RT-qPCR) to quantify the mtDNA copy number of granulosa cells obtained from 43 women undergoing an in vitro fertilization (IVF)/intracytoplasmic sperm injection (ICSI) program. Results: According to our analysis, a significant correlation was observed between age and mtDNA copy number (r = −0.54, P < 0.001) and between age and AMH level (r = −0.48, P < 0.001) of the same individual. There was also a positive correlation between mtDNA copy number and AMH (r = 0.88, P < 0.001) with AMH level falling as mtDNA decreases. In our regression, age and AMH were shown to have low collinearity (VIF = 1.297) but only AMH was correlated with mtDNA quantity (P < 0.001). Conclusion: Our study suggests that both mtDNA and AMH abundance are influenced by age and that AMH levels independently affect mtDNA copy number regardless of age. Further research is required to understand the role of AMH on mitochondria bioenergetics.