Big data quality is all about ensuring that the huge amounts of data are accurate, reliable, and useful. It is important because decisions made based on this data can affect many things, like business strategies, customer experiences, and even public policies. Many researchers are studying data quality in the context of big data. This study aims to analyze the research trends and patterns within the domain of big data quality. This method reveals hidden themes in large datasets, helping to understand data quality better. The findings show that Latent Dirichlet Allocation (LDA) is effective for topic modeling in big data, highlighting data quality challenges and opportunities. The research identified key trends and effective assessment methods. For researchers, using LDA in a systematic review helps summarize existing studies and find gaps, guiding future research. Practitioners and future researchers get useful direction for managing data quality and improving efficiency and decisions in various industries.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has acquired multiple mutations since its emergence. Analyses of the SARS-CoV-2 genomes from infected patients exhibit a bias toward C-to-U mutations, which are suggested to be caused by the apolipoprotein B mRNA editing enzyme polypeptide-like 3 (APOBEC3, A3) cytosine deaminase proteins. However, the role of A3 enzymes in SARS-CoV-2 replication remains unclear. To address this question, we investigated the effect of A3 family proteins on SARS-CoV-2 replication in THP-1 cells lacking A3A to A3G genes. The Wuhan, BA.1, and BA.5 variants had comparable viral replication in parent and A3A-to-A3G-null THP-1-ACE2 cells. On the other hand, the replication and infectivity of these variants were abolished in A3A-to-A3G-null THP-1-ACE2 cells in a series of passage experiments over 20 days. In contrast to previous reports, we observed no evidence for A3-induced SARS-CoV-2 mutagenesis in the passage experiments. Furthermore, our analysis of a large number of publicly available SARS-CoV-2 genomes did not reveal conclusive evidence for A3-induced mutagenesis. Taken together, our studies suggest that A3 family proteins can positively contribute to SARS-CoV-2 replication, however this effect is deaminase-independent.