The POPIA Code of Conduct for Research, as it is currently being considered, pertains to research conducted in South Africa, which, as part of the research process, uses personal information as defined under POPIA. This Discussion Document outlines the main areas relating to the processing of personal information for research purposes which the proposed Code will address, including what consent models would be permissible under POPIA; the issues in relation to genetic research and the processing of personal information contained in inherited characteristics; the use of information matching programmes by researchers; and the use of personal information obtained from social media platforms for research. With ongoing and wide consultation with the scientific community in South Africa and all relevant stakeholders, it is hoped that the Code will provide guidance in supporting the lawful and responsible use of personal information while conducting scientific research in South Africa. The purpose and scope of the Code of Conduct for Research are set out in the accompanying Commentary available at https://doi.org/10.17159/sajs.2021/10935

Background: Availability and access to the detection of resistance to anti-tuberculosis drug sremains a significant challenge in Malawi due to limited diagnostic services. The Xpert® MTB/RIF can detect Mycobacterium tuberculosis and resistance to rifampicin in a single, rapid assay. Rifampicin-resistant M. tuberculosis has not been well studied in Malawi.Objectives: We aimed to determine mutations in the rifampicin resistance determining region (RRDR) of the rpoB gene of M. tuberculosis strains which were defined as resistant to rifampicin by the Xpert MTB/RIF assay.Methods: Rifampicin-resistant isolates from 43 adult patients (≥ 18 years) from various districts of Malawi were characterised for mutations in the RRDR (codons 507–533) of the rpoB gene by DNA sequencing.Results: Mutations were found in 37/43 (86%) of the resistant isolates in codons 511, 512, 513,516, 522, 526 and 531. The most common mutations were in codons 526 (38%), 531 (29.7%) and 516 (16.2%). Mutations were not found in 6/43 (14%) of the resistant isolates. No novel rpoB mutations other than those previously described were found among the rifampicin-resistant M. tuberculosis complex strains.Conclusion: This study is the first to characterise rifampicin resistance in Malawi. The chaintermination DNA sequencing employed in this study is a standard method for the determination of nucleotide sequences and can be used to confirm rifampicin resistance obtained using other assays, including the Xpert MTB/RIF. Further molecular cluster analysis, such as spoligotyping and DNA finger printing, is still required to determine transmission dynamics and the epidemiological link of the mutated strains.

Characterization of HIV-1 from slow progressors is important to facilitate vaccine and antiviral drug development. To identify virus attenuations that may contribute to slower rates of disease progression, the full-length viral genomes from primary isolates of six slow progressing HIV-positive children were sequenced. Proviral DNA was extracted from cocultured peripheral blood mononuclear cells and used to PCR amplify, sequence, and extensively analyze the near full-length genomes and LTR regions. All primary HIV-1 isolates were HIV-1 subtype C throughout their genome, and amino acid (AA) sequence analysis revealed open reading frames for all genes. However, all isolates had at least one unusual gene/protein. For example, isolate LT5 had a 2AA insertion in the Vpr mitochondriotoxic domain. Isolate LT21 contained an additional 5AA in the C-terminus of tat exon 2, while integrase in isolate LT39 had an additional 4AA at the C-terminus. Rev from isolates LT45 and LT46 did not have the characteristic subtype C 16AA truncation, and in addition, had a further 3AA. Furthermore, altered functional domains were noted in several isolates, such as the cAMP-dependent kinase PKA phosphorylation site in Nef (LT5), a Vpr mutation involved in decreased proapoptotic activity (all isolates), and the Nef ExxxLL motif involved in the interaction with AP-1 and AP-2 (LT46). The slower HIV-1 disease progression in these six children may be attributed to altered protein functions. For example, LT46 Nef is unable to bind AP-1 and AP-2 and therefore is inactive on CD4 endocytosis. The biological relevance of these findings requires further investigation.

Jerome Amir Singh's affiliation was erroneously given as: Centre for Medical Ethics and Law, Stellenbosch University, Stellenbosch, South Africa. Thecorrect affiliation is: School of Law, Howard College, University of KwaZulu-Natal, Durban, South Africa. The error appears in the Discussion Document by Adams et al. [https://doi.org/10.17159/sajs.2021/10933] on Page 1 under Affiliations (no. 22) and on Page 11 in the table under Authors' information, as well as in the accompanying Commentary by Adams et al. [https://doi.org/10.17159/sajs.2021/10935] in Table 1 on Page 3.

Reports show that up to 30% of antiretroviral drug-naive patients in Johannesburg have CXCR4-utilizing HIV-1 subtype C. We assessed whether HIV-1 subtype C-infected individuals failing highly active antiretroviral therapy (HAART) have a higher proportion of CXCR4-utilizing viruses compared to antiretroviral drug-naive patients. The V3 loop was sequenced from plasma from 100 randomly selected HAART-failing patients, and tropism was established using predictive algorithms. All patients harbored HIV-1 subtype C with at least one antiretroviral drug resistance mutation. Viral tropism prediction in individuals failing HAART revealed similar proportions (29%) of X4-utilizing viruses compared to antiretroviral drug-naive patients (30%). Findings are in contrast to reports from Durban in which 60% of HAART-failing subjects harbored X4/dual/mixed-tropic viruses. Despite differences in proportions of X4-tropism within South Africa, the high proportion of thymidine analogue mutations (TAMs) and CXCR4-utilizing HIV-1 highlights the need for intensified monitoring of HAART patients and the predicament of diminishing drug options, including CCR5 antagonists, for patients failing therapy.