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N-acetylcysteine lacks universal inhibitory activity against influenza A viruses.

Garigliany MM, Desmecht DJ - J Negat Results Biomed (2011)

Bottom Line: N-acetylcysteine (NAC) has been recently proposed as an adjuvant therapeutic drug for influenza pneumonia in humans.In this study, we show that NAC is unable to alter the course of a fatal influenza pneumonia caused by inoculation of a murinized swine H1N1 influenza virus.Therefore, susceptibility of influenza viruses to NAC appears to be strain-dependent, suggesting that it cannot be considered as a universal treatment for influenza pneumonia.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pathology, Faculty of Veterinary Medicine, University of Liège, Belgium. mmgarigliany@ulg.ac.be

ABSTRACT
N-acetylcysteine (NAC) has been recently proposed as an adjuvant therapeutic drug for influenza pneumonia in humans. This proposal is based on its ability to restrict influenza virus replication in vitro and to attenuate the severity of the disease in mouse models. Although available studies were made with different viruses (human and avian), published information related to the anti-influenza spectrum of NAC is scarce. In this study, we show that NAC is unable to alter the course of a fatal influenza pneumonia caused by inoculation of a murinized swine H1N1 influenza virus. NAC was indeed able to inhibit the swine virus in vitro but far less than reported for other strains. Therefore, susceptibility of influenza viruses to NAC appears to be strain-dependent, suggesting that it cannot be considered as a universal treatment for influenza pneumonia.

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Effect of N-Acetylcysteine on swine H1N1 virus replication in Vero cells. Vero cells were infected with A/swine/Iowa/4/1976 (H1N1) at a MOI of 0.01. N-acetylcysteine treatment was started 1 hour post-infection and continued up to 48 hours post-infection. Viral titers were determined 48 hours post-infection. Data represent the mean ± SD of two independent experiments.
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Figure 3: Effect of N-Acetylcysteine on swine H1N1 virus replication in Vero cells. Vero cells were infected with A/swine/Iowa/4/1976 (H1N1) at a MOI of 0.01. N-acetylcysteine treatment was started 1 hour post-infection and continued up to 48 hours post-infection. Viral titers were determined 48 hours post-infection. Data represent the mean ± SD of two independent experiments.

Mentions: To examine this hypothesis further, the susceptibility to NAC of our porcine H1N1 strain was assessed in vitro by mimicking Geiler and colleagues methodological approach [4]. We also found a dose-dependent inhibition of influenza virus replication by NAC (Figure 3). However, even a very high dose (2.5 mg/ml, about 15 mM) resulted in a ≈ 6-fold reduction of virus yield, which is far less than that observed with H5N1 [4]. Thus, the anti-influenza activity of NAC appears to be strain-dependent as already supposable from previous studies [4]. The porcine A/swine/Iowa/4/1976 (H1N1) strain used here seems more resistant to NAC than the human strains A/PR/8/1934 (H1N1) and A/Hong Kong/8/1968 (H3N2) used by other authors in mouse models [2,3,8,10]. The lack of protection in vivo recorded in our experimental conditions is therefore probably associated to a combination of the NAC-resistance phenotype and to the pathotype [7] of the virus strain used.


N-acetylcysteine lacks universal inhibitory activity against influenza A viruses.

Garigliany MM, Desmecht DJ - J Negat Results Biomed (2011)

Effect of N-Acetylcysteine on swine H1N1 virus replication in Vero cells. Vero cells were infected with A/swine/Iowa/4/1976 (H1N1) at a MOI of 0.01. N-acetylcysteine treatment was started 1 hour post-infection and continued up to 48 hours post-infection. Viral titers were determined 48 hours post-infection. Data represent the mean ± SD of two independent experiments.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3104374&req=5

Figure 3: Effect of N-Acetylcysteine on swine H1N1 virus replication in Vero cells. Vero cells were infected with A/swine/Iowa/4/1976 (H1N1) at a MOI of 0.01. N-acetylcysteine treatment was started 1 hour post-infection and continued up to 48 hours post-infection. Viral titers were determined 48 hours post-infection. Data represent the mean ± SD of two independent experiments.
Mentions: To examine this hypothesis further, the susceptibility to NAC of our porcine H1N1 strain was assessed in vitro by mimicking Geiler and colleagues methodological approach [4]. We also found a dose-dependent inhibition of influenza virus replication by NAC (Figure 3). However, even a very high dose (2.5 mg/ml, about 15 mM) resulted in a ≈ 6-fold reduction of virus yield, which is far less than that observed with H5N1 [4]. Thus, the anti-influenza activity of NAC appears to be strain-dependent as already supposable from previous studies [4]. The porcine A/swine/Iowa/4/1976 (H1N1) strain used here seems more resistant to NAC than the human strains A/PR/8/1934 (H1N1) and A/Hong Kong/8/1968 (H3N2) used by other authors in mouse models [2,3,8,10]. The lack of protection in vivo recorded in our experimental conditions is therefore probably associated to a combination of the NAC-resistance phenotype and to the pathotype [7] of the virus strain used.

Bottom Line: N-acetylcysteine (NAC) has been recently proposed as an adjuvant therapeutic drug for influenza pneumonia in humans.In this study, we show that NAC is unable to alter the course of a fatal influenza pneumonia caused by inoculation of a murinized swine H1N1 influenza virus.Therefore, susceptibility of influenza viruses to NAC appears to be strain-dependent, suggesting that it cannot be considered as a universal treatment for influenza pneumonia.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Pathology, Faculty of Veterinary Medicine, University of Liège, Belgium. mmgarigliany@ulg.ac.be

ABSTRACT
N-acetylcysteine (NAC) has been recently proposed as an adjuvant therapeutic drug for influenza pneumonia in humans. This proposal is based on its ability to restrict influenza virus replication in vitro and to attenuate the severity of the disease in mouse models. Although available studies were made with different viruses (human and avian), published information related to the anti-influenza spectrum of NAC is scarce. In this study, we show that NAC is unable to alter the course of a fatal influenza pneumonia caused by inoculation of a murinized swine H1N1 influenza virus. NAC was indeed able to inhibit the swine virus in vitro but far less than reported for other strains. Therefore, susceptibility of influenza viruses to NAC appears to be strain-dependent, suggesting that it cannot be considered as a universal treatment for influenza pneumonia.

Show MeSH
Related in: MedlinePlus