On 2017 Aug 11, Alex Vasquez commented:

The concern being addressed (after the documentation of human DNA, at least in fragmented form) is whether or not such “vaccine DNA” could be incorporated into the living “human DNA” of the host recipient; however, that is only one rather minor concern with the injection of human DNA from one person’s cells into the body of another living human being. From an immunology and inflammology standpoint, the concern is the likelihood that exogenous human DNA would trigger inflammatory responses after being perceived by the immune system and received by receptors for DAMPs (damage associated molecular patterns). Whether this amount of inflammation triggered from human DNA in vaccines is great or small, frequent or uncommon is unknown due to the lack of adequate vaccine testing; however, one would expect it to be of greater consequence in “genetically susceptible” persons and also when co-administered in various mixtures with other vaccines and with their pro-inflammatory ingredients such as aluminum (which exacerbates the release of human DNA[1]), mercury (known to promote immune sensitization) and allergenic antibiotics common in vaccines, including streptomycin[2], polymyxin B[3], neomycin[4], gentamicin and kanamycin[5].

[1] "Although DNA DAMPs are closely associated with the development of autoimmune disease, DNA DAMPs also contribute to the activation of acquired immune responses following vaccination with alum adjuvant. Previous studies have shown that genomic DNA from dying cells induces the maturation of antigen-presenting cells as well as antigen-specific antibody and cytotoxic T cell responses. This suggests that self-DNA DAMPs can activate innate immune responses that induce acquired immunoresponses. Recently, Marichal et al. demonstrated that the adjuvanticity of alum was dependent on self-DNA released from cells at the alum inoculation site (Marichal et al., 2011). NLRP3 appears to be a key sensor in the induction of alum-mediated innate immunity, although its function is only partially dependent upon alum adjuvanticity. " Jounai et al. Recognition of damage-associated molecular patterns related to nucleic acids during inflammation and vaccination. Front Cell Infect Microbiol. 2013 Jan 8;2:168 [2] Romano et al. Anaphylaxis to streptomycin. Allergy. 2002 Nov;57(11):1087-8 [3] Henao MP, Ghaffari G. Anaphylaxis to polymyxin B-trimethoprim eye drops. Ann Allergy Asthma Immunol. 2016 Apr;116(4):372 [4] Goh CL. Anaphylaxis from topical neomycin and bacitracin. Australas J Dermatol. 1986 Dec;27(3):125-6 [5] Sánchez-Pérez et al. Allergic contact dermatitis from gentamicin in eyedrops, with cross-reactivity to kanamycin but not neomycin. Contact Dermatitis. 2001 Jan;44(1):54

On 2015 Jul 12, Kenneth Rochel de Camargo commented:

One would expect that after the Wakefield debate editors would be doubly cautious before publishing something that hypothesises a link between vaccines and autism. Unfortunately, this article shows it is not the case. The argument is woven out of strenuous "just so" links, without adequate justification for any of the many steps required to make the purported connection; how those tiny base sequences were established to be of human origin? how to make sure that those were not simply integrated into the viral genome? how does such a small sequence of pairs would interfere with a host? has it really been demonstrated that such small sequences can somehow enter host cells? But even if we take those at face value, the fundamental premise of the whole argument, the supposedly "epidemiologic" evidence, is anything but. The "evidence" is a graph that plots the average incidence of autism in three countries and the average MMR coverage in those countries, with absolutely no attempt at any statistical correlation. Once again, even if we take such data for its face value, it is mind boggling that anyone would attempt to call this "evidence". Why those three countries were selected? Why was the US, where this problem is even more serious, left out? Why not test for correlation within each country? Why not test for correlation at all? Given the problems we already have with vaccine coverage in many places of the world, it is utterly irresponsible to publish something that weak and claim it to be evidence of anything.

On 2015 Jul 12, Kenneth Rochel de Camargo commented:

One would expect that after the Wakefield debate editors would be doubly cautious before publishing something that hypothesises a link between vaccines and autism. Unfortunately, this article shows it is not the case. The argument is woven out of strenuous "just so" links, without adequate justification for any of the many steps required to make the purported connection; how those tiny base sequences were established to be of human origin? how to make sure that those were not simply integrated into the viral genome? how does such a small sequence of pairs would interfere with a host? has it really been demonstrated that such small sequences can somehow enter host cells? But even if we take those at face value, the fundamental premise of the whole argument, the supposedly "epidemiologic" evidence, is anything but. The "evidence" is a graph that plots the average incidence of autism in three countries and the average MMR coverage in those countries, with absolutely no attempt at any statistical correlation. Once again, even if we take such data for its face value, it is mind boggling that anyone would attempt to call this "evidence". Why those three countries were selected? Why was the US, where this problem is even more serious, left out? Why not test for correlation within each country? Why not test for correlation at all? Given the problems we already have with vaccine coverage in many places of the world, it is utterly irresponsible to publish something that weak and claim it to be evidence of anything.

On 2017 Aug 11, Alex Vasquez commented:

The concern being addressed (after the documentation of human DNA, at least in fragmented form) is whether or not such “vaccine DNA” could be incorporated into the living “human DNA” of the host recipient; however, that is only one rather minor concern with the injection of human DNA from one person’s cells into the body of another living human being. From an immunology and inflammology standpoint, the concern is the likelihood that exogenous human DNA would trigger inflammatory responses after being perceived by the immune system and received by receptors for DAMPs (damage associated molecular patterns). Whether this amount of inflammation triggered from human DNA in vaccines is great or small, frequent or uncommon is unknown due to the lack of adequate vaccine testing; however, one would expect it to be of greater consequence in “genetically susceptible” persons and also when co-administered in various mixtures with other vaccines and with their pro-inflammatory ingredients such as aluminum (which exacerbates the release of human DNA[1]), mercury (known to promote immune sensitization) and allergenic antibiotics common in vaccines, including streptomycin[2], polymyxin B[3], neomycin[4], gentamicin and kanamycin[5].

[1] "Although DNA DAMPs are closely associated with the development of autoimmune disease, DNA DAMPs also contribute to the activation of acquired immune responses following vaccination with alum adjuvant. Previous studies have shown that genomic DNA from dying cells induces the maturation of antigen-presenting cells as well as antigen-specific antibody and cytotoxic T cell responses. This suggests that self-DNA DAMPs can activate innate immune responses that induce acquired immunoresponses. Recently, Marichal et al. demonstrated that the adjuvanticity of alum was dependent on self-DNA released from cells at the alum inoculation site (Marichal et al., 2011). NLRP3 appears to be a key sensor in the induction of alum-mediated innate immunity, although its function is only partially dependent upon alum adjuvanticity. " Jounai et al. Recognition of damage-associated molecular patterns related to nucleic acids during inflammation and vaccination. Front Cell Infect Microbiol. 2013 Jan 8;2:168 [2] Romano et al. Anaphylaxis to streptomycin. Allergy. 2002 Nov;57(11):1087-8 [3] Henao MP, Ghaffari G. Anaphylaxis to polymyxin B-trimethoprim eye drops. Ann Allergy Asthma Immunol. 2016 Apr;116(4):372 [4] Goh CL. Anaphylaxis from topical neomycin and bacitracin. Australas J Dermatol. 1986 Dec;27(3):125-6 [5] Sánchez-Pérez et al. Allergic contact dermatitis from gentamicin in eyedrops, with cross-reactivity to kanamycin but not neomycin. Contact Dermatitis. 2001 Jan;44(1):54