Dear Colleagues,

Infections caused by viruses play an increasing role in human and animal medicine. Even after a century of our quest for antimicrobial drugs, we still have very few antiviral drugs for use in the treatment of serious and life-threatening viral infections. There is no specific treatment for most of the viral families causing diseases, and medical personnel are left with a narrow choice of supportive treatment and the hope that the infected host can mount an immune response robust enough to lead to a favorable outcome for the patient. We have some successful vaccines that can prevent some of the previously widespread viral diseases, which have been either eradicated or brought under control by the vaccination. Nevertheless, the major force in defeating most viral infections is the immune response of the infected organism. Thus, the key to understanding mechanisms of viral diseases from the perspective of disease outcome is to deepen our knowledge about the interaction of the infecting virus and the host immune response.

There are some viruses, such as HIV, in which this interaction has been extensively studied—mostly because, for example, the HIV virus infects the immune system itself. Yet, after more than 30 years of study, the exact immune correlates of the successful immune response are not clearly understood. However, this is almost a lone example, because the immune correlates of most viral diseases have not been studied at all, or our knowledge is only superficial.

For this Special Issue, we invite all papers focusing on the effect of viruses on the immune system, as well as their interaction and correlates of the immune system defense against infecting viruses. We also encourage studies which define the molecular correlates of virus virulence, as these may define the severity of infections, resistance to antivirals, and potentially immune escape variants.

Prof. Dr. Pavel Bostik
Dr. Shubhada Bopegamage
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Microorganisms is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2000 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

• virulence
• molecular typing
• immunity
• antivirals
• human viruses

Identification of new mixed variants in the epidemiological analysis of SARS-CoV-2 genomic sequences from different regions of India

Whole-genome sequencing of Severe Acute Respiratory Syndrome Coronavirus -2 (SARS-CoV-2) has helped to identify the geographic distribution of the different virus clades and their variants across the globe. The availability of genomic sequences helps in understanding different nucleotides as well as amino acid variations fixed in their genetic make-up.

This study presents an analysis of 696 SARS-CoV-2 genomic sequences from different parts of India, in a period between January to August 2020. This work reveals three key facts: i) Predominance of ‘G’ clade and its variants (GH and GR) in different states of India, ii) three mixed SARS-CoV-2 clade variants (G-S, GR-GV, and GH-GR) were specifically identified to be circulating in India, iii) Further, a unique variant has been identified by amino acid changes in the ORF1ab region, described here as ‘CI2’ (a B.4 variant).

Overall, the observed nucleotide variation in the SARS-CoV-2 genome is less than 1% as compared to the original L clade of Wuhan, China. However, the sequence divergence detected within a short frame of time suggests that SARS-CoV-2 is continuously evolving towards host adaptation. Continuous genomic surveillance is essential to understand the virus evolution and its effects on disease transmission dynamics, host adaptation, and disease pathophysiology.

Dynamics of immune status indicators in HIV-infected individuals with M.tuberculosis co-infection

Abstract :Tuberculosis (TB) and HIV have profound effects on the immune system, which can lead to the activation of viral replication and negatively regulate the activation of T cells. Dysregulation in the production of cytokines necessary to fight HIV and M. tuberculosis may ultimately affect the results of the treatment and be important in the pathogenesis of HIV infection and TB.

The work presents the results of study of HIV co-infection impact on the plasma levels of pro- and anti- inflammatory cytokines (IFN-γ, TNF-α, IL-2, IL-4, IL-6, IL-8, IL-10, IL-18, IL-1RA) in patients with dual infection HIV/TB in the process of receiving antiretroviral (ART) and TB -treatment versus the cohort of patients with HIV monoinfection and TB monoinfection.

The reduced levels of  most pro- and –anti-inflammatory cytokines in patients with dual infection indicate a prolonged dysregulation of immune response and suggests a less effective immune reconstitution which increase disease severity in pulmonary/extrapulmonary TB in HIV/TB patients. The exception was cytokines IL-6, Il-8 and IL-1RA. The secretion of those cytokines was significantly higher in HIV/TB patients compared with patients with HIV monoinfection and TB monoinfection. The high levels of IL-6 (9.8-11.3-fold increase) persisted in patients with HIV/TB even after 6 months of therapy which could explain an increased risk of cardiovascular complications, chronic diseases of the gastrointestinal tract and kidneys among that cohort of patients. In HIV/TB patients with a fatal outcome, increased levels of IL-8 (5.2-fold increase) were observed in comparison with the surviving patients. When studying the levels of IL-1RA expression, it was found that in a group of patients with HIV/TB co-infection, this indicator was on average almost 4 times higher than in patients with HIV and TB only, but it significantly decreased after 1.5-2 months of double therapy. However, the exception was HIV/TB patients who had the development of inflammatory immune recovery syndrome (IRIS). Those patients did not have a decrease in the level of IL-1RA expression and this indicator remained high throughout the entire duration of therapy. Based on the received data elevated IL-6, IL-8 and IL-1RA levels may serve as a potential biomarker of treatment outcome.