Abstract

Viruses are spherical particles of size 50–500 nm. The genome (DNA or RNA) of viruses is typically encapsulated by a protein shell, known as, capsid which is further coated by a protein-rich lipid bilayer for enveloped viruses. Most non-enveloped viruses have a rigid capsid with a high structural symmetry such as icosahedral, helical, and complex. The capsid and envelope proteins are part of the structural proteins of viruses and provide distinct structural features. A major function of these structural proteins is determining the binding of viruses to host cells and these structural proteins are the most exposed on the viral surface. While viruses are simple biological nanoparticles devoid of genetic machinery, they can replicate once they enter a host cell. This is a multistep process starting with the interaction of the viral surface proteins with specific molecules of a cell surface. It is well established that virus particles must evade or cross through the 1.5-μm-thick proteoglycan shield surrounding a cell to reach the plasma membrane of the cell. Viruses have evolved to interact with the proteoglycans and receptors of the plasma membrane to trigger signals for endocytosis or membrane fusion, processes essential for cellular entry (Figure 1). Despite the fact that viruses can intrude multiple tissues and organs of a host, the infection predominates in specific organs and cell types. This is determined by the specific interaction of the viral surface proteins with the proteoglycans and plasma membrane receptors.

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