Since the emergence of SARS-CoV-2, the virus that causes coronavirus disease (COVID-19) in late 2019, communities have been required to rapidly adopt community mitigation strategies rarely used before, or only in limited settings. This study aimed to examine the attitudes and beliefs of Australian adults towards the COVID-19 pandemic, and willingness and capacity to engage with these mitigation measures. In addition, we aimed to explore the psychosocial and demographic factors that are associated with adoption of recommended hygiene-related and avoidance-related behaviors. A national cross-sectional online survey of 1420 Australian adults (18 years and older) was undertaken between the 18 and 24 March 2020. The statistical analysis of the data included univariate and multivariate logistic regression analysis. The survey of 1420 respondents found 50% (710) of respondents felt COVID-19 would ‘somewhat’ affect their health if infected and 19% perceived their level of risk as high or very high. 84·9% had performed ≥1 of the three recommended hygiene-related behaviors and 93·4% performed ≥1 of six avoidance-related behaviors over the last one month. Adopting avoidance behaviors was associated with trust in government/authorities (aOR: 6.0, 95% CI 2.6–11·0), higher perceived rating of effectiveness of behaviors (aOR: 4·0, 95% CI: 1·8–8·7), higher levels of perceived ability to adopt social distancing strategies (aOR: 5.0, 95% CI: 1·5–9.3), higher trust in government (aOR: 6.0, 95% CI: 2.6–11.0) and higher level of concern if self-isolated (aOR: 1.8, 95% CI: 1.1–3.0). In the last two months, members of the public have been inundated with messages about hygiene and social (physical) distancing. However, our results indicate that a continued focus on supporting community understanding of the rationale for these strategies, as well as instilling community confidence in their ability to adopt or sustain the recommendations is needed.

Background: Hepatitis B virus (HBV) is an infectious disease of global significance, causing a significant health burden in Africa due to complications associated with infection, such as cirrhosis and liver cancer. In Nigeria, which is considered a high prevalence country, estimates of HBV cases are inconsistent, and therefore additional clarity is required to manage HBV-associated public health challenges.Methods: A systematic review of the literature (via PubMed, Advanced Google Scholar, African Index Medicus) was conducted to retrieve primary studies published between 1 January 2010 and 31 December 2019, with a random-effects model based on proportions used to estimate the population-based prevalence of HBV in the Nigerian population.Results: The final analyses included 47 studies with 21,702 participants that revealed a pooled prevalence of 9.5%. A prevalence estimate above 8% in a population is classified as high. Sub-group analyses revealed the highest HBV prevalence in rural settings (10.7%). The North West region had the highest prevalence (12.1%) among Nigeria’s six geopolitical zones/regions. The estimate of total variation between studies indicated substantial heterogeneity. These variations could be explained by setting and geographical region. The statistical test for Egger’s regression showed no evidence of publication bias (p = 0.879).Conclusions: We present an up-to-date review on the prevalence of HBV in Nigeria, which will provide critical data to optimise and assess the impact of current prevention and control strategies, including disease surveillance and diagnoses, vaccination policies and management for those infected.

Background: As immunisation program launches have previously demonstrated, it is essential that careful planning occurs now to ensure the readiness of the public for a COVID-19 vaccine. As part of that process, this study aimed to understand the public perceptions regarding a future COVID-19 vaccine in Australia. Methods: A national cross-sectional online survey of 1420 Australian adults (18 years and older) was undertaken between 18 and 24 March 2020. The statistical analysis of the data included univariate and multivariable logistic regression model analysis. Results: Respondents generally held positive views towards vaccination. Eighty percent (n = 1143) agreed with the statement that getting myself vaccinated for COVID-19 would be a good way to protect myself against infection. Females (n = 614, 83%) were more likely to agree with the statement than males (n = 529, 78%) (aOR = 1.4 (95% CI: 1.1–1.8); P = 0.03), while 91% of those aged 70 years and above agreed compared to 76% of 18–29-year-olds (aOR = 2.3 (95% CI:1.2–4.1); P = 0.008). Agreement was also higher for those with a self-reported chronic disease (aOR = 1.4 (95% CI: 1.1–2.0); P = 0.04) and among those who held private health insurance (aOR = 1.7 (95% CI: 1.3–2.3); P < 0.001). Beyond individual perceptions, 78% stated that their decision to vaccinate would be supported by family and friends. Conclusion: This study presents an early indication of public perceptions towards a future COVID-19 vaccine and represents a starting point for mapping vaccine perceptions. To support an effective launch of these new vaccines, governments need to use this time to understand the communities concerns and to identify the strategies that will support engagement.

Many pathogens, including viruses, bacteria, and protozoan parasites, suppress cellular immune responses through activation of type I IFN signaling. Recent evidence suggests that immune suppression and susceptibility to the malaria parasite, Plasmodium, is mediated by type I IFN; however, it is unclear how type I IFN suppresses immunity to blood-stage Plasmodium parasites. During experimental severe malaria, CD4⁺ Th cell responses are suppressed, and conventional DC (cDC) function is curtailed through unknown mechanisms. Here, we tested the hypothesis that type I IFN signaling directly impairs cDC function during Plasmodium infection in mice. Using cDC-specific IFNAR1-deficient mice, and mixed BM chimeras, we found that type I IFN signaling directly affects cDC function, limiting the ability of cDCs to prime IFN-γ–producing Th1 cells. Although type I IFN signaling modulated all subsets of splenic cDCs, CD8^– cDCs were especially susceptible, exhibiting reduced phagocytic and Th1-promoting properties in response to type I IFNs. Additionally, rapid and systemic IFN-α production in response to Plasmodium infection required type I IFN signaling in cDCs themselves, revealing their contribution to a feed-forward cytokine-signaling loop. Together, these data suggest abrogation of type I IFN signaling in CD8^– splenic cDCs as an approach for enhancing Th1 responses against Plasmodium and other type I IFN–inducing pathogens.

Tumor necrosis factor (TNF) is critical for controlling many intracellular infections, but can also contribute to inflammation. It can promote the destruction of important cell populations and trigger dramatic tissue remodeling following establishment of chronic disease. Therefore, a better understanding of TNF regulation is needed to allow pathogen control without causing or exacerbating disease. IL-10 is an important regulatory cytokine with broad activities, including the suppression of inflammation. IL-10 is produced by different immune cells; however, its regulation and function appears to be cell-specific and context-dependent. Recently, IL-10 produced by Th1 (Tr1) cells was shown to protect host tissues from inflammation induced following infection. Here, we identify a novel pathway of TNF regulation by IL-10 from Tr1 cells during parasitic infection. We report elevated Blimp-1 mRNA levels in CD4⁺ T cells from visceral leishmaniasis (VL) patients, and demonstrate IL-12 was essential for Blimp-1 expression and Tr1 cell development in experimental VL. Critically, we show Blimp-1-dependent IL-10 production by Tr1 cells prevents tissue damage caused by IFNγ-dependent TNF production. Therefore, we identify Blimp-1-dependent IL-10 produced by Tr1 cells as a key regulator of TNF-mediated pathology and identify Tr1 cells as potential therapeutic tools to control inflammation. Many parasitic diseases are associated with the generation of potent inflammatory responses. These are often needed to control infection, but can also cause tissue damage if not appropriately regulated. IL-10 has emerged as an important immune regulator that protects tissues by dampening inflammation. Recently, some T cells that initially produce inflammatory cytokines have been found to start producing IL-10 as a mechanism of auto-regulation. We identified an important transcriptional regulator called B lymphocyte-induced maturation protein 1 (Blimp-1), which promotes IL-10 production by IFNγ-producing CD4⁺ T (Tr1) cells during malaria and visceral leishmaniasis, two important diseases caused by protozoan parasites. We found that Tr1 cell-derived IL-10 suppressed anti-parasitic immunity, but played a critical role in preventing tissue damage caused by the potent pro-inflammatory cytokine TNF. Specifically, IL-10 protected macrophages from TNF-mediated destruction, and this enabled lymphocytes to continue to migrate to regions in the spleen where T and B cell responses are generated. These findings allow us to better understand how parasites persist in a host, but also identify new opportunities to control inflammation to prevent disease.

The development of immunoregulatory networks is important to prevent disease. However, these same networks allow pathogens to persist and reduce vaccine efficacy. Here, we identify type I interferons (IFNs) as important regulators in developing anti-parasitic immunity in healthy volunteers infected for the first time with Plasmodium falciparum. Type I IFNs suppressed innate immune cell function and parasitic-specific CD4+ T cell IFNγ production, and they promoted the development of parasitic-specific IL-10-producing Th1 (Tr1) cells. Type I IFN-dependent, parasite-specific IL-10 production was also observed in P. falciparum malaria patients in the field following chemoprophylaxis. Parasite-induced IL-10 suppressed inflammatory cytokine production, and IL-10 levels after drug treatment were positively associated with parasite burdens before anti-parasitic drug administration. These findings have important implications for understanding the development of host immune responses following blood-stage P. falciparum infection, and they identify type I IFNs and related signaling pathways as potential targets for therapies or vaccine efficacy improvement.