Virology Research Journal

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Commentary - Virology Research Journal (2022) Volume 6, Issue 1

Pathophysiology of viral protein and interaction with receptors on infected cell.

Wilson Pereyra*

Department of Veterinary Medicine, Faculty of Medicine, Federal University of Juiz de Fora, Brazil

*Corresponding Author:

Wilson Pereyra
Department of Veterinary Medicine
Federal University of Juiz de Fora
E-mail: [email protected]

Received: 27-Dec-2021, Manuscript No. AAVRJ-22-53991; Editor assigned: 29-Dec-2021, PreQC No. AAVRJ-22-53991(PQ); Reviewed: 12-Jan-2022, QC No. AAVRJ-22-53991; Revised: 18-Jan-2022, Manuscript No. AAVRJ-22-53991(R); Published: 25-Jan-2022, DOI:10.35841/AAVRJ-6.1.103

Citation: Pereyra W. Pathophysiology of viral protein and interaction with receptors on infected cell. Virol Res J. 2022; 6(1):103

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Virus–receptor intuitive play a key administrative part in viral have extend, tissue tropism, and viral pathogenesis. Infections utilize rich techniques to join to one or different receptors, overcome the plasma layer boundary, enter, and get to the vital have cell apparatus. The viral connection protein can be seen as the “key” that opens have cells by association with the “lock”—the receptor—on the cell surface, and these lock-and-key intuitive are basic for infections to effectively attack have cells. Numerous common subjects have developed in virus–receptor utilization inside and over infection families illustrating that infections regularly target specific classes of atoms in arrange to intervene these occasions. Common viral receptors incorporate sialylated glycans, cell grip particles such as immunoglobulin superfamily individuals and integrins, and phosphatidylserine receptors. The repetition in receptor utilization recommends that infections target specific receptors or “common locks” to require advantage of their cellular work conjointly recommends developmental preservation. Due to the significance of starting infection intelligent with have cells in viral pathogenesis and the repetition in viral receptor utilization, misuse of these procedures would be an appealing target for unused antiviral therapeutics.


Viral attachment, Viral signalling, Viral entry, Igsf receptors.


Acknowledgment and intelligent with cellular receptors may be a basic starting step within the irresistible viral life cycle and plays a key administrative part in have extend, tissue tropism, and viral pathogenesis. Infections are commit intracellular pathogens that depend on have cell apparatus in arrange to carry out an irresistible life cycle and eventually spread to unused have cells. Hence, infections utilize exquisite procedures to coordinate connection to one or different receptors to cross the plasma film and get to the vital have cell apparatus. The viral connection protein can be seen as the “key” that opens the cells by collaboration with the lock—the receptor—on the host-cell surface, starting basic downstream steps within the viral life cycle. Viral receptors work not as it were as connection moieties but too as section components, facilitators of viral trafficking, and activators of signaling occasions, and in numerous cases, infections utilize numerous receptors to carry out diverse capacities with life cycle [1,2]. Infection diseases actuate a proinflammatory reaction counting expression of cytokines and chemokines. The consequent leukocyte enlistment and antiviral effector capacities contribute to the primary line of defense against infections. The atomic virus-cell intuitive starting these occasions have been examined expectation, and it shows up that viral surface glycoproteins, double-stranded RNA, and intracellular viral proteins all have the capacity to actuate flag transduction pathways driving to the expression of cytokines and chemokines. The signaling pathways enacted by viral diseases incorporate the major proinflammatory pathways, with the translation figure NF-κB having gotten uncommon consideration. These translation variables in turn advance the expression of particular inducible have proteins and take an interest within the expression of a few viral qualities [3].

Here we survey the current information of virus-induced flag transduction by seven human pathogenic infections and the foremost broadly utilized exploratory models for viral diseases. The atomic mechanisms of virus-induced expression of cytokines and chemokines is additionally analyzed. A trademark of a viral disease is an intense response by the contaminated cell. This incorporates actuation of a preexisting antiviral defense apparatus, commitment to apoptosis, and generation of particular cytokines. These occasions contribute to the decrease of viral replication and to the confinement of viral spread. By centering on a few vital human pathogenic infections as well as broadly utilized research facility models for viral diseases, this content will audit the current information of which viral components are capable for actuating cytokine generation and the components through which this happens [4].

Instantly taking after a viral disease, a solid have reaction is started. For a run of infections it has presently been clarified that the insignificant interaction of viral surface proteins with cellular surface proteins begins a cellular response that in numerous cases leads to the primary wave of cytokine generation after disease. With regard to cytokine acceptance, a few of the foremost vital flag transduction pathways actuated by infections are appeared. Intergalactic (IFN) administrative and IRF-7 are as of late found virus-activated translation components that have been credited an vital part in IFN-α/β expression. These translation components ended up enacted by serine/threonine phosphorylation.

The mitogen-activated protein (Outline) kinases p38 and Jun N-terminal kinase (JNK) are moreover actuated in reaction to numerous infections. This translation calculate is regularly found within the cytoplasm complexed with an inhibitory protein, IκB, of which different isoforms exist. Upon contamination, signaling occasions are started driving to enactment of Outline kinase kinase kinases (MAP3K), which advance the enactment of a expansive kinase complex able to phosphorylate IκB at two particular amino-terminal serine buildups. The kinases capable for IκB phosphorylation are IκB kinase α (IKK α) and IKK β. Phosphorylated IκB is in this way focused on for corruption through the ubiquitin-dependent 26S proteasome pathway. Debasement of IκB unmasks the atomic localization flag of NF-κB, which at that point moves to the core and actuates translation [5].


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