Peroxiredoxin 2 (PRDX2) is upregulated in various cancers including oral squamous cell carcinoma (OSCC). It is a known tumor promoter in some cancers, but its role in OSCC is unclear. This study aimed to investigate the effect of arecoline, an alkaloid of the betel nut, and human papillomavirus type 16 (HPV16) E6/E7 oncoproteins on induction of PRDX2 expression, and also the effects of PRDX2 overexpression in oral cell lines. Levels of PRDX2 protein were determined using western blot analysis of samples of exfoliated normal oral cells (n = 75) and oral lesion cells from OSCC cases (n = 75). Some OSCC cases were positive for HPV infection and some patients had a history of betel quid chewing. To explore the level of PRDX2 by western blot, the proteins were extracted from oral cell lines that were treated with arecoline or retroviruses containing HPV16 E6 gene and HPV16 E6/E7 expressing vector. For analysis of PRDX2 functions, cell proliferation, cell-cycle progression, apoptosis and migration was compared between oral cells overexpressing PRDX2 and cells with PRDX2-knockdown. PRDX2 expression levels tended to be higher in OSCC samples that were positive for HPV infection and had history of betel quid chewing. Arecoline treatment in vitro at low concentrations and overexpression of HPV16 E6 or E6/E7 in oral cells induced PRDX2 overexpression. Interestingly, in oral cells, PRDX2 promoted cell proliferation, cell-cycle progression (G2/M phase), cell migration and inhibited apoptosis. Upregulation of PRDX2 in oral cells was induced by arecoline and HPV16 oncoproteins and promoted growth of OSCC cells.

Co-infection with multiple DENV serotypes can affect human immune status and complicate the clinical presentation and management of dengue patients, so understanding the prevalence and dynamics of co-infection is important for effective dengue control. We aimed to identify and characterize DENV co-infection patterns in field-caught mosquitoes and dengue patients. This study was conducted in northeastern Thailand between June 2016 to August 2019. Female Aedes mosquitos collected from and around dengue patient’s houses were analyzed for DENV infection and presence of serotypes using RT-PCR. DENV serotyping was successful in 154 (39.49%) of human and 165 (14.26%) of mosquito samples. Prevalence of DENV co-infection in patients and mosquitoes was 22.73% (35 cases) and 28.48% (47 samples), respectively. Co-infection with multiple serotypes were double (human 88.57%, mosquito 89.36%), triple (human 5.72%, mosquito 10.64%) and quadruple (human 5.72%, mosquito 0%) infections. Concurrent infection was different between hosts and concurrence patterns of DENV serotype in each host mostly composed of the predominant serotype of the detected year. This is the first report that show DENV co-infection patterns in field-caught mosquito and in dengue fever patients with combinations of triple and quadruple serotypes in Thailand. These finding are potentially useful for understanding shifts in serotypes, concurrent DENV infection patterns, vaccine development, and further research on the ability of vectors to transmit multiple serotypes.

Chlamydia trachomatis is a common agent of sexually transmitted infection, especially in asymptomatic extra-genital sites among men who have sex with men (MSM). This study aims to investigate anatomical site distribution and genotypes of C. trachomatis from asymptomatic MSM in northeast Thailand. Specimens were collected using swabs from anorectal, oropharyngeal, and urethral sites in 346 asymptomatic MSM. C. trachomatis infection was determined by real-time polymerase chain reaction and genotyping was based on sequences of the ompA gene. The results showed that infection by C. trachomatis was most common at the urethral site (29.1%, 101/346) followed by oropharyngeal (17.6%, 61/346) and anorectal site (17.0%, 59/346). In addition, C. trachomatis infection was significantly associated with absence of condom use (odds ratio = 1.909, 95%CI = 1.054–3.457, P = 0.033) at the urethral site. Overall 49.4% (171/346) of individuals were infected in at least one site. Infection at only the anorectum, oropharynx, or urethra was seen in 9.0, 9.3, and 18.5% of participants, respectively. Concurrent infections at anorectum/oropharynx, anorectum/urethra, oropharynx/urethra, and all three sites were 2.0, 4.3, 4.6, and 1.7%, respectively. Genotype D predominated at the anorectal and urethral sites among asymptomatic MSM in northeast Thailand. Concurrent infection in two or three anatomical sites occurred. C. trachomatis screening at all three sites in asymptomatic MSM is important and should be considered for proper treatment and prevention of transmission.

Background and Objectives: Cervical cancer is one of the most common types of frequently found cancers in Thailand. One of the causative agents is the infection of the high-risk human papillomavirus (HPV) type 16 and 18. Traditional medicines are rich sources of bioactive compounds which are a valuable source for the development of novel cancer therapies. In this study, the therapeutic effects of 3 traditional medicines, Kerra^TM, KS^TM, and Minoza^TM, were studied on HeLa and CaSki cells. Materials and Methods: The effects of Kerra^TM, KS^TM, and Minoza^TM on cancer cells were evaluated through cytotoxicity and cell death assays. The infection assay using HPV-16 pseudovirus was also carried out. Results: All traditional medicines efficiently suppressed cell growths of HeLa and CaSki, with Kerra^TM being the most potent anticancer agent followed by KS^TM and Minoza^TM. Kerra^TM at 158 µg/mL and 261 µg/mL significantly increases the percentage inhibition of the HPV-16 pseudovirus infection in a pre-attachment step in a dose-dependent manner, while KS^TM at 261 µg/mL efficiently inhibited viral infection in both pre-attachment and adsorption steps. However, Kerra^TM, KS^TM, and Minoza^TM at subtoxic concentrations could not reduce the viral E6 mRNA expressions of HPV-16 and HPV-18. Cell death assay by acridine orange/ethidium bromide showed that Kerra^TM increased population of dead cells in dose-dependent manner in both CaSki and HeLa. The percentage of secondary necrosis in Kerra^TM-treated CaSki was higher than that of HeLa cells, while the percentage of late apoptotic cells in HeLa was higher than that of CaSki, indicating that HeLa was more susceptible to Kerra^TM than CaSki. For KS^TM and Minoza^TM, these extracts at 250 µg/mL promoted autophagy over cell death. At 500 µg/mL, the percentage of dead cells in Kerra^TM was higher than that of KS^TM and Minoza^TM. Conclusions: Kerra^TM is a potent traditional medicine for promoting cancer cell death. Kerra^TM is possibly useful in the prevention and treatment of cervical cancer. Further investigation will be carried out to gain a better understanding of the biochemical mechanism and the pharmacological activity underlying this effect.

Commercial herbal compounds are a main attractive target to explore for a novel drug for the treatment of HSV. This study investigated the anti-HSV infectivity of extracts derived from the Thai commercial herbals Kerra^TM, KS^TM, and Minoza^TM. Wild-type HSV-1 KOS, HSV-2, and drug-resistant HSV-1 dxpIII were used to investigate any inhibitory effects of these extracts. A plaque formation assay was performed to investigate the effects of all extracts. The viral ICP4, UL30, gD, and gB and cellular IL1β, IL6, STAT3, and NFKB1 expression levels were evaluated. The Kerra^TM, KS^TM, and Minoza^TM extracts at 50–200 μg/mL significantly inhibited HSV-1 KOS and dxpIII infection in the post-entry step, whereas only Minoza^TM could not reduce plaque formation of HSV-2. In addition, ICP4, UL30, and gD mRNAs and gB protein were significantly decreased in Kerra^TM- and KS^TM-treated cells. Furthermore, IL1B, IL6, STAT3, and NFKB1 expression was upregulated in Kerra^TM- and KS^TM-treated cells. Kerra^TM and KS^TM could be agents against HSV infection, especially the HSV acyclovir (ACV)-resistant strain. From the docking result and drug-likeness prediction, 2-Methoxy-9H-xanthen-9-one, piperine, and sargassopenilline D found in Kerra^TM, KS^TM, and Minoza^TM show high binding energy closely resembling ACV, and are desirable as drug-like characteristics.

Ellagic acid (EA) is a phenolic phytochemical found in many plants and their fruits. Vaginal epithelial cells are the first line of defense against pathogen invasion in the female reproductive tract and express antimicrobial peptides, including hBD2 and SLPI. This study investigated the in vitro effects of EA (1) on vaginal innate immunity using human vaginal epithelial cells, and (2) on HPV16 pseudovirus infection. Vaginal cells were cultured in the presence or absence of EA, and the expression of hBD2 and SLPI was determined at both transcriptional and translational levels. In addition, secretion of various cytokines and chemokines was measured. Cytotoxicity of EA was determined by CellTiter-blue and MTT assays. To investigate the ability of EA to inhibit HPV16 infection, EA was used to treat HEK-293FT cells in pre-attachment and adsorption steps. We found significant increases in both hBD2 mRNA (mean 2.9-fold at 12.5 µM EA, p < 0.001) and protein (mean 7.1-fold at 12.5 µM EA, p = 0.002) in response to EA. SLPI mRNA also increased significantly (mean 1.4-fold at 25 µM EA, p = 0.01), but SLPI protein did not. Secretion of IL-2 but not of other cytokines/chemokines was induced by EA in a dose-dependent manner. EA was not cytotoxic. At the pre-attachment step, EA at CC₂₀ and CC₅₀ showed a slight trend towards inhibiting HPV16 pseudovirus, but this was not significant. In summary, vaginal epithelial cells can respond to EA by producing innate immune factors, and at tested concentrations, EA is not cytotoxic. Thus, plant-derived EA could be useful as an immunomodulatory agent to improve vaginal health.