Tag: Viral infections

Fig. 1. Differential sensitivity of EV A B to IFN-y in various cell types and Cell type and correlation with NO production. (A) Cells were cultured for 18 hours with or without recombinant IFN--y, infected with EV, and assayed for infectious progeny virus 24 hours later (23). Progeny virus is expressed as the mean ± SEM of log10 viral titer in triplicate cultures minus log10 of infectious virus recovered from parallel cultures 1 hour after the addition of virus to the culture. (B) Accumulation of NO2- in the medium of the same cell cultures, measured by the Griess assay (8). Results, presented as the mean ± SEM of triplicate cultures, were similar in each of two or three additional experiments with each cell type. Source: Karupiah, 1993.

The ability of IFN-gamma to inhibit replication of viruses correlated with the cells’ production of nitric oxide (NO).

Interferons induce the expression of hundreds of antiviral genes. Interferons notably stimulate inducible nitric oxide synthase (NOS), thus, the production of large amounts of nitrogen oxyde (NO). A 1993 study by Karupiah et al. (1), that appears to be still factually correct, found that the activity of iNOS is both necessary and sufficient for a substantial antiviral effect of IFN-gamma in vitro.

Models for Th1 differentiation. (Part a of the Figure 1). Source: Weaver, 2007.

The Th1-Th2 paradigm provides a framework for understanding T cell biology and the interplay of innate and adaptive immunity.

The roles and interactions of Th1, Th2 and Th17 immunity is a fascinating piece of physiological literacy with implications in the treatment of viral infections, allergies and autoimmune disorders. Weaver and colleagues, 2007 (1), produced a quality review on the topic. In the article below, we shared our notes and several curated citation from the review by Weaver and colleagues (1) as well as from other sources.