Aflatoxin B1 (AFB1) contamination of food is very high in most sub-Saharan African countries. AFB1 is known to cause hepatocellular carcinoma (HCC) by inducing mutation in the tumour suppressor gene TP53. The number of new HCC cases is high in West Africa with an accompanying high mortality. The type I interferon (IFN) pathway of the innate immune system limits viral infections and exerts its anti-cancer property by up-regulating tumour suppressor activities and pro-apoptotic pathways. Indeed, IFN-α is reported to show significant protective effects against hepatic fibrogenesis and carcinogenesis. However, the mechanism behind AFB1 deregulation of the type I interferon (IFN) signalling pathway, with consequent HCC is largely unknown. This current study seeks to test the hypothesis that AFB1 inhibits the type I IFN response by directly interfering with key signalling proteins and thus increase the risk of HCC in humans. We evaluated the effects of AFB1 on the type I IFN signalling pathway using IFN stimulated response element (ISRE)-based luciferase reporter gene assay. In addition, the effects of AFB1 on the transcript levels of JAK1, STAT1 and OAS3 were assessed by real-time quantitative polymerase chain reaction (RT-qPCR) and confirmed by immunoblot assay. Our results indicated that AFB1 inhibited the type I IFN signalling pathway in human hepatoma cell line HepG2 cells by suppressing the transcript levels of JAK1, STAT1 and OAS3. AFB1 also decreased the accumulation of STAT1 protein. The inhibition of the type I IFN anti-cancer response pathway by AFB1 suggest a novel mechanism by which AFB1 may induce hepatocellular carcinoma in humans.

Background: Chikungunya is now of public health concern globally due to its re-emergence in endemic areas and introduction into new areas of the world. Worldwide, the vectors for transmission of the chikungunya virus are Aedes mosquitoes and these are prevalent in Ghana. Despite its global significance, the true burden of chikungunya virus infection in Ghana is largely unknown and the threat of outbreak remains high owing to international travel. This study sought to determine chikungunya virus infection among febrile patients suspected of having malaria infections at some selected health facilities in the Ashanti, Bono East, and Bono Regions of Ghana. Methodology: This cross-sectional study recruited six hundred (600) febrile patients suspected of having malaria who submitted their clinical samples to the laboratories of the selected health facilities for the diagnosis of their infections. Five to ten millilitres (5-10ml) of venous blood were collected from each study participant. Sera were separated and tested for anti-chikungunya (IgM and IgG) antibodies using InBios ELISA kit following the manufacturer’s instruction. Samples positive for chikungunya IgM and IgG were selected and tested for chikungunya virus RNA using Reverse Transcription-quantitative Polymerase Chain Reaction. Malaria Rapid Diagnostic Test kits were used to screen the participants for malaria. Structured questionnaires were administered to obtain demographic and clinical information of the study participants. Result: Of the 600 samples tested, the overall seroprevalence of chikungunya was 6%. The seroprevalence of chikungunya IgM and IgG antibodies were 1.8% and 4.2% respectively. None of the chikungunya IgM and IgG positive samples tested positive for chikungunya RNA by RT-qPCR. Of the 600 samples, tested 32.3% (194/600) were positive for malaria parasites. Malaria and chikungunya co-infection was detected in 1.8% (11/600) of the participants. Conclusion: Findings from the current study indicate low-level exposure to the chikungunya virus suggesting the virus is circulating and potentially causing morbidity in Ghana.

Diarrhoeal diseases are among the most frequent causes of morbidity and mortality in children worldwide, especially in sub-Saharan Africa. This case–control study was conducted to investigate the bacterial, viral and parasitic pathogens associated with acute diarrhoea among children attending three health facilities in Kumasi, Ghana. Stool specimens were collected from 240 children under 5 years of age visiting hospitals in Kumasi, Ghana due to acute diarrhoea and from 107 healthy controls of similar age. Both intestinal and malaria parasites were diagnosed by microscopy whereas rota- and adenoviruses were identified by stool antigen immunochromatograhic testing. Bacterial enteropathogens were detected by conventional culture techniques. Of all subjects, 23 (6.6%) were positive for malaria parasitaemia, 139 (40.1%) had at least one bacterial agent in their stool and 25 (7.2%) had ova or parasites. Subjects infected with malaria had the highest odds of having diarrhoea [12.0 (95% CI 1.56, 92.35)] followed by those with rotaviruses [4.4 (95% CI 2.05, 9.47)] and bacterial infection [4.99 (95% CI 1.45, 17.17)]. In conclusion, this study was unique as it looked at the three groups of pathogens (parasites, viruses and bacteria) that cause acute diarrhoea in children in the Kumasi metropolis of Ghana. This study has shown for the first time since 2004 that malaria parasitaemia, rotavirus and bacterial infections still remain common pathogens associated with acute childhood diarrhoea in the Kumasi metropolis of Ghana.

Hepatitis B vaccination is the most effective preventive measure in reducing the incidence of chronic hepatitis B virus (HBV) infection and its consequences such as cirrhosis, hepatocellular carcinoma, liver failure and death. Ghana introduced the universal HBV vaccination in the national Expanded Programme on Immunization in 2002. The current study sought to determine the sero-protection rate and the prevalence of HBV infection among fully vaccinated children in the West Gonja District in the Savanna Region of Ghana. This cross-sectional study recruited three hundred and fifty (350) fully vaccinated children who visited West Gonja Catholic Hospital from September to December 2019 for healthcare. Structured questionnaires were administered to obtain information on the demographics. The clinical history of the participants was obtained from the hospital records. Sera were separated from 2-5ml of blood sample collected from each participant after informed consent had been sought from their parents/guardians. Sera were tested for HBsAg, anti-HBs and anti-HBc using ELISA. Samples positive for HBsAg or anti-HBc were tested for HBV DNA by Real-Time Polymerase Chain Reaction. The overall sero-protection rate (anti-HBs titers ≥ 10 mIU/mL) among the studied participants was 56% with anti-HBs geometric mean titer (GMT) of 95.7 mIU/mL (± 6.0; 95% CI) compared with GMT of 2.8 mIU/mL (± 0.2; 95% CI) among non-seroprotected participants. There was no statistically significant difference in sero-protection rate between males and females (p-value = 0.93) and in relation to age (p-value = 0.20). The prevalence of HBV infection among studied participants as determined by the HBV DNA/HBsAg positivity was 1.4% while anti-HBc sero-positivity was 2%. Even though the sero-protection rate and HBV infection rate reported in the current study compares with that of other international studies further studies need to be conducted to understand the factors related to sero-protection and HBV infection rate in the Savanna Region of Ghana.

The type I interferon signaling pathway of the innate immune system plays a key role in the first line of defense in eliminating pathogens and other chemical agents that are introduced into the body and is also known to exhibit the anticancer properties. Therefore, any agent being chemical or components of microorganisms that tend to inhibit or suppress the type I interferon response pathway will weaken the innate immune system and predispose individuals to infectious agents and cancers. Aflatoxin B1 has been reported to modulate the immune system by suppressing inflammatory cytokines, monocytes, lymphocytes and the type I interferon signaling response pathway. Aflatoxin B1 contamination of food is very high in most sub-Saharan African countries. Aflatoxin B1 contamination of diet coupled with subsequent prolonged heavy exposure is one of the major risk factors for the development of hepatocellular carcinoma. Aflatoxin B1 is known to cause hepatocellular carcinoma by inducing mutation in the tumor suppressor gene TP53. We present in this review the mechanism by which aflatoxin B1 inhibits the type I interferon signaling pathway thus pre-disposing exposed individuals to cancers and other infections.

Type 1 interferons (IFN-1) are pleiotropic cytokines with well-established anticancer and antiviral properties, particularly in mucosal tissues. Hence, natural IFN-1-inducing treatments are highly sought after in the clinic. Here, we report for the first time that cryptolepine, a pharmacoactive alkaloid in the medicinal plant Cryptolepis sanguinolenta, is a potent IFN-1 pathway inducer. Cryptolepine increased the transcript levels of JAK1, TYK2, STAT1, STAT2, IRF9, and OAS3, as well as increased the accumulation of STAT1 and OAS3 proteins, similar to recombinant human IFN-α. Cryptolepine effects were observed in multiple cell types including a model of human macrophages. This response was maintained in MAVS and STING-deficient cell lines, suggesting that cryptolepine effects are not mediated by nucleic acids released upon nuclear or organelle damage. In agreement, cryptolepine did not affect cell viability in concentrations that triggered potent IFN-1 activation. In addition, we observed no differences in the presence of a pharmacological inhibitor of TBK1, a pleiotropic kinase that is a converging point for Toll-like receptors (TLRs) and nucleic acid sensors. Together, our results demonstrate that cryptolepine is a strong inducer of IFN-1 response and suggest that cryptolepine-based medications such as C. sanguinolenta extract could be potentially tested in resource-limited regions of the world for the management of chronic viral infections as well as cancers.