Chronic HIV-1 infection can cause neurological illness, also known as HIV-associated neurocognitive disorders (HAND). The elevated level of pro-inflammatory cytokines and chemokines, such as C-C Chemokine Ligand 5 (CCL5/RANTES), is one of the ways of causing HIV-1-mediated neuroinflammation. C-C Chemokine Receptor 5 (CCR5) is the main coreceptor for viral entry into host cells and for mediating induction of CCL5/RANTES. CCR5 and CCL5 are part of a correlated axis of immune pathways used for effective protection against the HIV-1 virus. The purpose of this paper was to review the literary knowledge about the immunopathological relationship between this immune complex and neuroAIDS. A systematic review of the literature was conducted based on the selection and search of articles, available in English, Spanish, or Portuguese in the time frame of 1990–2022, of primary and secondary types in the PUBMED, Science Direct, SciELO, and LILACS databases through descriptors (MeSH) together with “AND”: “CCR5”; “CCL5”; “neurological manifestations”; or “HIV”. The methodological quality of the articles was assessed using the JBI Checklists and the PRISMA 2020 writing guidelines were followed. A total of 36 articles were included in the final composition of the review. The main cells of the CNS affected by neuroAIDS are: neurons; microglia; astrocytes; and oligodendrocytes. Molecular devices and their associations with cellular injuries have been described from the entry of the virus into the host’s CNS cell to the generation of mental disorders. Furthermore, divergent results were found about the levels of CCL5/RANTES secretion and the generation of immunopathogenesis, while all condensed research for CCR5 indicated that elevation of this receptor causes more neurodegenerative manifestations. Therefore, new therapeutic and interventional strategies can be conditioned on the immunological direction proposed in this review for the disease.

As the host’s first line of defense against pathogens, Toll-like receptors (TLRs), such as the TLR3, are genes encoding transmembrane receptors of the same name. Depending on their expression, TLRs cause a pro- or anti-inflammatory response. The purpose of the article was to determine whether there is an association between the Toll-like receptor 3 (TLR3) rs3775291 Single Nucleotide Polymorphism—SNP and susceptibility to infections. This review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) 2020 guidelines and was registered in PROSPERO under the code CRD42023429533. A systematic search for relevant studies was performed using PubMed, Scopus, SciELO, Google Scholar, and Science Direct by the MeSH descriptors and the Boolean Operator “AND”: “Infections”; “TLR3”; “SNP”, between January 2005 and July 2022. Summary odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were calculated for genotypic comparison assuming a dominant genetic model (CT + TT vs. CC). A meta-analysis of 18 studies consisting of 3118 cases and 4368 controls found a significant association for risk between the presence of the TLR3 SNP rs3775291 and infections as part of the general analysis (OR = 1.16, 95% CI = 1.04–1.28, p = 0.004). In the subgroups of continents, the SNP had a protective role in Europe for 1044 cases and 1471 controls (OR = 0.83, 95% CI = 0.70–0.99, p = 0.04); however, the Asian (for 1588 patients and 2306 controls) and American (for 486 patients and 591 controls) continents had an increase in infectious risk (OR = 1.37, 95% CI = 1.19–1.58, p < 0.001; OR = 1.42, 95% CI = 1.08–1.86, and p = 0.01, respectively). Heterogeneity between studies was detected (I² = 58%) but was explained in meta-regression by the subgroup of continents itself and publication bias was not evident. The results of the meta-analysis suggest a significant association between the TLR3 rs3775291 polymorphism and susceptibility to infections. Thus, when analyzing subgroups, the Asian and American continents showed that this SNP confers a higher risk against infections in a dominant genotypic model. Therefore, more studies are necessary to fully elucidate the role of TLR3 rs3775291 in infections.

COVID-19 is an infectious disease caused by coronavirus 2 of the severe acute syndrome (SARS-CoV-2). Single nucleotide polymorphisms (SNPs) in genes, such as TLR2, responsible for an effective human immune response, can change the course of infection. The objective of this article was to verify associations between epidemiological factors and TLR2 SNP rs3804100 (Thymine [T] > Cytosine [C]) in professionals from Health Institutions (HI) who worked during the first pandemic wave and COVID-19. A case-control study was conducted with Belém-PA HI workers (Northern Brazil), divided into symptomatology groups (Asymptomatic-AS; n = 91; and Symptomatic-SI; n = 123); and severity groups classified by Chest Computerized Tomography data (symptomatic with pulmonary involvement—SCP; n = 35; symptomatic without pulmonary involvement—SSP; n = 8). Genotyping was performed by Sanger sequencing, and Statistical Analysis was conducted through the SPSS program. Bioinformatics servers predicted the biological functions of the TLR2 SNP. There were associations between the presence of comorbidities and poor prognosis of COVID-19 (especially between symptomatology and severity of COVID-19 and overweight and obesity) and between the sickness in family members and kinship (related to blood relatives). The homozygous recessive (C/C) genotype was not found, and the frequency of the mutant allele (C) was less than 10% in the cohort. No significant associations were found for this SNP in this cohort. The presence of SNP was indicated to be benign and causes a decrease in the stability of the TLR2 protein. These data can help the scientific community and medicine find new forms of COVID-19 containment.

The COVID-19 pandemic represented a huge obstacle for public health and demonstrated weaknesses in surveillance and health promotion systems around the world. Its etiological agent, SARS-CoV-2, of zoonotic origin, has been the target of several studies related to the control and prevention of outbreaks and epidemics of COVID-19 not only for humans but also for animals. Domestic animals, such as dogs and cats, have extensive contact with humans and can acquire the infection both naturally and directly from humans. The objective of this article was to summarize the seroprevalence findings of SARS-CoV-2 in dogs and cats and correlate them with the strength of infection risk between each of them. This is a systematic review and meta-analysis following the recommendations of PRISMA 2020. The search and selection of papers was carried out using in vivo experimental works with animals using the descriptors (MeSH/DeCS) “Animal”, “Public Health”, “SARS-CoV-2” and “Pandemic” (together with AND) in English, Portuguese or Spanish for Science Direct, PUBMED, LILACS and SciELO databases. The ARRIVE checklist was used for methodological evaluation and the Comprehensive Meta-Analysis v2.2 software with the Difference Risk (RD) test to evaluate statistical inferences (with subgroups by continent). Cats showed greater susceptibility to SARS-CoV-2 compared to dogs both in a joint analysis of studies (RD = 0.017; 95% CI = 0.008–0.025; p < 0.0001) and in the American subgroup (RD = 0.053; 95% CI = 0.032–0.073; p < 0.0001), unlike the lack of significant difference on the European continent (RD = 0.009; 95% CI = −0.001–0.018; p = 0.066). Therefore, it was observed that cats have a greater interest in health surveillance due to the set of biological and ecological aspects of these animals, but also that there are a set of factors that can influence the spread and possible spillover events of the virus thanks to the anthropozoonotic context.