Interferon In Viral Infections Research Articles

Elevated blood MxA protein levels in children with newly diagnosed B-ALL: A prospective case-control study

Background/Aim: Although leukemia is thought to be triggered or initiated by viral infections, it is not clear which viruses are the causative agents for which stage of the disease. Previous studies have shown that the MxA protein is expressed from blood mononuclear cells in reply to inducement of type I interferons in viral infections. Viral infections may trigger childhood B-cell acute lymphoblastic leukemia (B-ALL), and the hypothesis of this study was the detection of the presence of viral infection by measuring MxA expression in blood mononuclear cells of recently diagnosed pediatric B-ALL patients as a surrogate viral marker. Methods: This study consisted two groups; the study group consisted of 30 newly diagnosed B-ALL and the control group consisted of 29 healthy asymptomatic children of similar age. Proven bacterial infection and COVID-19 PCR positivity were exclusion criteria. Bacterial culture of peripheral blood, complete blood count, plasma CRP levels and whole blood MxA levels detected by ELISA (Enzyme-Linked ImmunoSorbent Assay) method were taken. Results: The patients’ mean age was 7.42 years in the leukemia group (previously mentioned as study group) and 7.25 years in the control group. Routine serologic studies for newly diagnosed leukemia patients (CMV, EBV VCA and Hepatitis B IgM, anti-HCV and anti-HIV) were negative in all patients without any bacterial infection detected. The MxA levels were found significantly higher in children with B-ALL than in control group (5.84 (2.18-199.38) and 2.45 (1.17-88.65) ngr/ml, respectively, with P

The mode of action of interferons in viral infections and their possible role in the control of hepatitis B

Interferons can alter the course of virus infections by inhibiting virus replication at the intracellular level and by modifying the aspecific and specific immune response to viral antigens in body fluids and on cellular surfaces. Treatment of isolated cells with interferon renders them resistant to infections by viruses belonging to virtually any family. Knowledge of the mechanism of this effect is derived from studies employing both DNA (especially vaccinia virus and SV40) and RNA-viruses (especially picorna-, toga-, rhabdo-, reo- and retroviruses). Interferon induces multiple alterations in the level and state of intracellular regulatory molecules, leading to inhibition of virus replication at several possible steps. In the case of certain DNA viruses, transcription of viral DNA seems to be inhibited. In the case of RNA viruses the target for interferon action is mainly translation. The retroviridae constitute a special case and, in view of their analogy with the hepadnaviridae, are of particular relevance to the possible effects of interferon on the replication of HBV. Interferon inhibits one or more initial stages of primary infection of cells by transforming or nontransforming retroviruses, thereby preventing or delaying the synthesis and/or integration of viral DNA. In cells that already contain an integrated and fully expressed retrovirus genome, interferon treatment results in a reduced release of viral particles as well as a downward shift of the ratios between the numbers of infectious vs noninfectious particles. Immuno-modulatory properties of interferon which might alter the course of HBV-infection include: potentiation of cytotoxic activity of lymphocytes and macrophages; direct anti-inflammatory effects; enhancement or depression in antibody formation.(ABSTRACT TRUNCATED AT 250 WORDS)

The role of interferon in viral infections

Interferon, a product of mammalian tissues, was originally described as an antiviral agent over twenty years ago. Only in the past few years has evidence started to accumulate that interferon actually played a role in vivo in natural virus infections. Initially, evidence was accumulated showing that interferon could inhibit the replication of many viruses in vitro. The interferon, through induction of a second antiviral protein, could inhibit in vitro viral transcription or translation. Later, indirect evidence for an effect of interferon on in vivo viral infections was obtained by showing that (a) a temporal relationship existed between the appearance of interferon in viral infections and the progress of the infection and (b) treatment of virally infected animals with exogenous interferon or interferon inducer often resulted in less severe infections. The most recent and direct evidence for a role for interferon in natural viral infections involves the use of an anti-interferon globulin. In several cases, injection of the anti-interferon globulin into animals infected with a wide variety of viruses resulted in a severely altered course of infection. These studies suggest that interferon is directly involved in the progress of viral infections. The involvement of the interferon in the viral infections could be a direct effect of the interferon on viral replication, or an interaction of the interferon with other host defenses, such as the immune system.

From the NIH: Appearance of interferon in viral infections may cause asthma while controlling virus

From the NIH: Appearance of interferon in viral infections may cause asthma while controlling virus

Sensitivity of Human Foetal Intestine to Interferon

ACUTE infectious non-bacterial gastroenteritis is a common disease in which recovery usually occurs within 24–48 h of the onset of diarrhoea and vomiting1,2. This short duration suggests that a mechanism of rapid onset, such as interferon, may play a significant role in recovery. The role of interferon in recovery from acute enteric viral infections of man is, however, unknown. Indeed, little is known about the ability of the human intestine to either produce or respond to interferon. We have therefore investigated the role of interferon in viral infections of the human gut. We found that human foetal intestine is quite responsive to the antiviral properties of exogenous interferon, and when so treated exhibits a marked inhibition of the replication of an enteric virus, echovirus type 11.