Hi Samir,

It dépends on your NTM species. For MAC Fad2 and PPE genes were shown to be associated with virulence/survival.

PE/PPE genes in M. abscessus.

Oxidative stress proteins

there are several unknown proteins described too

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2887559/#r35

Note that some species of NTM can be polymorphic, there are rough and smouth colonies displaying different virulence.

 Dear Samir Das

Some of the virulence factors are common to both M. tuberculosis complex and some environmental mycobacteria such as

1. The intracellular location: All mycobacteria have the potential to reside inside phagocytic cells where they are protected from antibodies, complement and other components of the immune defence system.

2. Neutralisation of free radicals: To survive within phagocytes these bacteria must have the ability to block the host cell capacity to form toxic oxygen radicals or neutralise them as they are formed.

3. Mycobacteria have a lipid rich outer cell wall. Some of these lipids may have the ability to stimulate interleukin 1 (IL-1) and tumour necrosis factor alpha (TNF-alpha) release form macrophages that contribute to the symptoms of the illness.

4. Specific virulence genes have been mapped in a number of atypical mycobacterial species including M. abscessus and M. smegmatis which are considered to be analogues of Mycobacterium tuberculosis complex.

5. This amazing table from Ripoll F et al 2009 gives detailed comparison of the virulence factors between the three species.

(a) For proteins belonging to the PE/PPE and ESX families, homologs of M. tuberculosis LeuD, TrpD, ProC and PurC (amino acid and purine biosynthesis) present in both M. abscessus and M. smegmatis

(b) A protein homologous to IipB (Rv1478) is also present in both M. abscessus (MAB_2727c) and M. smegmatis (Msmeg_3156)

(c) A protein homologous to IrtB (Rv1349) is also present in both M. abscessus (MAB_2261c) and M. smegmatis (Msmeg_6553)

(d) There are three other proteins homologous to Rv3763 in M. abscessus: MAB_ 2379 (51% identity), MAB_3261c (35%) and MAB_4074c (34%)

(e) Presence of homologs most similar to non mycobacterial proteins

(f) A cluster similar to the narGHIJ cluster encoding the M. tuberculosis nitrate reductase is present in M. smegmatis, but not M. abscessus.

(g) There are three phospholipases C encoded in H37Rv: PlcA (Rv2351c), PlcB (Rv2350c) and PlcC (Rv2349c)

(h) Homologs of RpfB (Rv1009) and RpfC (Rv1884c) are present in both M. abscessus (MAB_1130 and MAB_4080c, respectively) and M. smegmatis (Msmeg_5439 and Msmeg_4640, respectively).

(i) Other M. tuberculosis sigma factors involved in virulence (SigA, SigD, SigE, SigH) have homologs in both M. abscessus and M. smegmatis.

Best wishes

Roshdi

Good day, Mr. Samir Das.

In nontuberculous mycobacteria (NTM), there are smooth and rough morphotypes based on their colony morphology. The genes, mps1, mbtH, and mmpL4b are associated with the synthesis and transport of glycopeptidolipid (GPL) which is found in the cell wall of the smooth morphotype. GPL is able to alter cellular functions through their interaction with the host receptors. When smooth morphotype transitions to a rough morphotype, there is a loss of expression of these genes causing the formation of corded colonies making them more virulent. Lack of GPL in rough morphotypes also has an impact on its intracellular survival. In rough morphotype, studies show that the trehalose polyphleates (TPP), found in their cell wall, have a function in the formation of corded colonies. papA3, pks, fadD23, and mmpL10 genes are associated with the synthesis and transport of TPP.

References:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5952384/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5524727/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2733780/

https://www.frontiersin.org/articles/10.3389/fmicb.2018.01145/full