Detection of influenza virus induced DNA damage by Comet assay

Lakshmi, A.N Vijaya; Ramana, M. Venkata; Vijayashree, B.; Ahuja, Y.R.; Sharma, Gita

doi:10.1016/s1383-5718(99)00058-3

Cited by 22 publications

(16 citation statements)

References 21 publications

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“…By analyzing DNA repair foci (as indicated by γH2AX), results here show that there is a significant increase in DNA strand breaks in host cells after influenza infection, both in vitro and in vivo . Extending upon reports that DNA is damaged during influenza infection in vitro [55,56], the studies presented here show that DNA damage not only occurs early in viral infection, but persists until long after the virus has cleared. Additionally, analysis of specific cell types shows that both lung epithelial cells and immune cells suffer DNA damage during the regenerative phase of infection.…”

Section: Discussionsupporting

confidence: 69%

Influenza infection induces host DNA damage and dynamic DNA damage responses during tissue regeneration

Parrish

Chan

et al. 2015

Cell. Mol. Life Sci.

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Influenza viruses account for significant morbidity worldwide. Inflammatory responses, including excessive generation of reactive oxygen and nitrogen species (RONS), mediate lung injury in severe Influenza infections. However, the molecular basis of inflammation-induced lung damage is not fully understood. Here, we studied influenza H1N1 infected cells in vitro, as well as H1N1 infected mice, and we monitored molecular and cellular responses over the course of two weeks in vivo. We show that influenza induces DNA damage both when cells are directly exposed to virus in vitro (measured using the comet assay) and also when cells are exposed to virus in vivo (estimated via γH2AX foci). We show that DNA damage, as well as responses to DNA damage, persist in vivo until long after virus has been cleared, at times when there are inflammation associated RONS (measured by xanthine oxidase activity and oxidative products). The frequency of lung epithelial and immune cells with increased γH2AX foci is elevated in vivo, especially for dividing cells (Ki-67 positive) exposed to oxidative stress during tissue regeneration. Additionally, we observed a significant increase in apoptotic cells as well as increased levels of DSB repair proteins Ku70, Ku86 and Rad51 during the regenerative phase. In conclusion, results show that influenza induces DNA both in vitro and in vivo, and that DNA damage responses are activated, raising the possibility that DNA repair capacity may be a determining factor for tissue recovery and disease outcome.

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Section: Discussionsupporting

confidence: 69%

Influenza infection induces host DNA damage and dynamic DNA damage responses during tissue regeneration

Parrish

Chan

et al. 2015

Cell. Mol. Life Sci.

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“…The enhancement of p53 activity in the presence of NS1 observed by Zhirnov may be due to the elevated DNA damage induced by wild-type influenza A virus. DNA breakage or damage is a common phenomenon during influenza A infection 34 and is the most important trigger of p53 activation. 35 Compared with wild-type influenza A virus, delNS1 virus always displays a reduced replication capability in host …”

Section: Effects Of H5n1-ns1 Variants On Ifn Induction Wz LI Et Al 239mentioning

confidence: 99%

Effects of NS1 variants of H5N1 influenza virus on interferon induction, TNFα response and p53 activity

Wang

Zhang

et al. 2010

Cell Mol Immunol

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Non-structural protein 1 (NS1) is an important virulence factor of the highly pathogenic H5N1 avian influenza virus. A five-amino-acid (5 aa) deletion at position 80-84 and an aspartic acid to glutamic acid substitution at position 92 (D92E) are two major NS1 mutations that are highly correlated with enhanced virulence. To investigate the effect of these mutations in H5N1 virulence, three H5N1-NS1 variants were constructed: NS51 (lacking 5 aa at position 80-84), NS51(I) (carrying a 5-aa insertion at position 80-84) and NS51(IM) (carrying both the 5-aa insertion and the D92E mutation). We examined the effects of these mutations on interferon (IFN) induction, tumor-necrosis factor (TNF)a response, p53 activity and apoptosis. We found that the D92E mutation eliminated NS1's repressive effect on IFN induction, while the 5-aa deletion resulted in enhanced resistance to TNFa responses. We also observed that all three variants exhibited a similar suppressive effect on p53 transcriptional activity, although none of them significantly influenced apoptosis of host cells. Our findings shed new light on the role of NS1 in the pathogenicity of H5N1 virus.

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“…In this study, the level of urinary 8-OhdG was significantly higher in H1N1 infected patients than in the control subjects. It has been reported that DNA damage is induced in human leucocytes infected by the influenza virus, and the DNA damage due to influenza virus infection is believed to be related to apoptosis (Vijaya et al, 1999;Wiwanitkit, 2010). Lipid peroxidation and protein oxidation were also increased in the plasma of H1N1 infected patients.…”

Section: Discussionmentioning

confidence: 99%

“…Among ROS, hydroxy radicals are powerful oxidizing agents that can react at a high rate with most organic and inorganic molecules in the cell, including DNA, proteins, lipids, amino acids, sugars, and metals (Kohen and Nyska, 2002). A number of studies concerned with oxidative damage, including DNA damage and lipid peroxidation caused by the influenza virus infection have been performed (Vijaya et al, 1999;Kumar et al, 2003;Nikam et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

Enhanced oxidative damage to DNA, lipids, and proteins and levels of some antioxidant enzymes, cytokines, and heat shock proteins in patients infected with influenza H1N1 virus

Lim¹,

Oh²,

Kim³

et al. 2014

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Summary. -Influenza virus is well known for pandemics and epidemics with high morbidity. Many studies have been focused to this problematics, however, oxidative damage to DNA, lipids, and proteins and the expression of cytokines, antioxidant enzymes and heat-shock proteins (HSPs) in H1N1 virus-infected patients has not been investigated yet. Therefore we aimed this study at these issues. We found out that patients infected with the 2011 H1N1 virus as compared to control subjects exhibited an increased oxidative damage to DNA, lipids and proteins as assayed by levels of 8-hydroxydeoxyguanosine (8-OhdG) and malondialdehyde (MDA) and carbonyl content in plasma and urine. Moreover, the levels of antioxidant enzymes SOD and catalase, cytokines Il-6, 1L-10 and TNF-α and HSPs 90 and 27 were also significantly higher in the H1N1-infected patients. Our results suggest that the influenza H1N1 virus is a strong inducer of (i) oxidative damage to DNA, lipids, and proteins, (ii) antioxidant enzymes, (iii) cytokines and (iv) HSPs.Keywords: influenza H1N1 virus; patients; oxidative damage; antioxidant enzymes; cytokines; heat-shock proteins * Corresponding authors. E-mail: dsul@korea.ac.kr, litjacob@chol. com; phone: +82-2-920-6614. # These authors contributed equally to this work. Abbreviations: 8-OhdG = 8-hydroxydeoxyguanosine; SOD = superoxide dismutase; IL = interleukin; TNF-α = tumor necrosis factor alpha; MDA = malondialdehyde; Prx = peroxiredoxin; HSPs = heat shock proteins; ROS = reactive oxygen species

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Detection of influenza virus induced DNA damage by Comet assay

Cited by 22 publications

References 21 publications

Influenza infection induces host DNA damage and dynamic DNA damage responses during tissue regeneration

Influenza infection induces host DNA damage and dynamic DNA damage responses during tissue regeneration

Effects of NS1 variants of H5N1 influenza virus on interferon induction, TNFα response and p53 activity

Enhanced oxidative damage to DNA, lipids, and proteins and levels of some antioxidant enzymes, cytokines, and heat shock proteins in patients infected with influenza H1N1 virus

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