NFKB1 and tuberculosis: Similar previous studies from our group have also shown the emergence of genetically altered viral quasi-species, having accumulated significantly higher frequency of high-risk drug resistance (DR) mutations in reverse transcriptase (RT) gene and additional copies of Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-kB) binding sites in the long terminal repeat (LTR) region of the genome of viral isolates from HIV-TB co-infected individuals, as compared to viral isolates from HIV mono-infected host [71,72].