The Viruses
Julius P. Kreier in Infection, Resistance, and Immunity, 2022
An outer envelope protects many types of viruses. The viral envelope is essentially a membrane derived from the host cell which consists of a lipid bilayer with inserted virus encoded proteins. Such proteins are usually glycosylated by host cell enzymes and appear as “spikes” on the viral surface when viewed by electron microscopy (e.g., Figures 16.1 B and 16.1C). Except for some members of the poxvirus family, all enveloped viruses lose their infectivity following extraction of their lipid with ethyl ether. Naked, nonenveloped viruses are unaffected by treatment with ether. Thus, enveloped virus particles are often labile and lose infectivity unless conditions are present to preserve the integrity of the viral envelope. In addition, enveloped viruses are usually more susceptible to detergents that disrupt the lipid envelope.
Tea Polyphenolic Compounds against Herpes Simplex Viruses
Satya Prakash Gupta in Cancer-Causing Viruses and Their Inhibitors, 2014
Herpesvirus particles can range from 120 to 300 nm in diameter, though many are approximately 200 nm in diameter. All herpesviruses contain several distinct morphological features, including core, capsid, tegument, and envelope. The core of a herpes virion consists of a linear, double-stranded DNA (dsDNA) genome arranged in toroid form, ranging from 120 to 230 kilobase pairs (kbp) in length; about 30–35 different proteins reside with the genome in the core. The core is protected by an icosahedral capsid composed of 150 hexons and 12 pentons, which has a diameter ranging from 100 to 110 nm. A tegument separates the inner capsid from the outer envelope; the tegument contains several proteins, some of which are present at up to 2000 copies. The viral envelope is composed of a lipid bilayer and contains various glycoprotein spikes (Kelly et al. 2009; Roizman and Baines 1991).
Neuropathogenesis of viral infections
Avindra Nath, Joseph R. Berger in Clinical Neurovirology, 2020
Occasionally, viral infections may trigger an immune response against host antigens. Such immune responses have been implicated in the pathogenesis of diseases such as post viral encephalomyelitis, multiple sclerosis, transverse myelitis and Gillian Barre syndrome [71]. Patients with herpes encephalitis may develop an autoimmune NMDA receptor encephalitis [72] and it is likely that other paraneoplastic antibodies will be recognized following viral brain infection. Viruses may trigger autoimmune responses by several different mechanisms [73]. Enveloped viruses as they exit the cell membrane may carry host antigens from the membrane which get incorporated into the viral envelope. These host antigens may now trigger an immune response. Alternatively, the viral proteins themselves may have sequence homology that is similar to host proteins. Hence, immune responses directed against the virus may also target the host proteins. This phenomenon has been termed “molecular mimicry” [74]. However, the immune responses may be perpetuated by “epitope spreading” as demonstrated in a Theiler’s murine encephalomyelitis model [75]. Additionally, virus infected cells can release small immunodominant peptides which can sensitize uninfected cells. These “by-stander sensitized” cells can then become targets for antigen specific immune responses by cytotoxic T cells [76].
Biochemical and immunological aspects of COVID-19 infection and therapeutical intervention of oral low dose cytokine therapy: a systematic review
Published in Immunopharmacology and Immunotoxicology, 2021
Ratheesh M, Sheethal S, Svenia P. Jose, Sony Rajan, Sulumol Thomas, Tariq Jagmag, Jayesh Tilwani
The structure of coronavirus consists of Spike (S), Membrane (M), Envelope (E) glycoproteins, Hemagglutinin esterase (HE) and nucleocapsid (N) protein (Figure 1). The viral envelope is a lipid bilayer in which the structural proteins, membrane (M), envelope (E) and spike (S) are anchored. There is also a shorter spike-like surface protein called Hemagglutinin esterase (HE) in the coronavirus subset (especially the members of betacoronavirus subgroup A) [7]. Previous studies reported that SARS-CoV-2 has close similarities with SAR-CoV. The S protein helps the virus to gain entry into the host cells and the surface unit of S protein will facilitate the binding of virus to the target receptor as well as priming of S protein by cellular protease. This permits the fusion of both viral and host cell membranes [8–10]. The similarity of SAR-CoV-2 with SARS-CoV shows that the novel coronavirus also uses the same Angiotensin converting enzyme 2 (ACE-2) receptor as its entry receptor and TMPRSS2 serine protease helps in S protein priming [11,12]. ACE 2 is a membrane protein which is present in almost all the organs but highly expressed in type 2 alveolar cells [13–15]. Likewise, it is also expressed on vascular endothelial cells and cardiac cells which may perhaps describe the cardiovascular complications that occur in some patients [5]. S protein of SARS-CoV-2 has high affinity to ACE-2 receptors and this helps the virus to be transmitted more effectively between humans [16,17].
COVID-19: a wreak havoc across the globe
Published in Archives of Physiology and Biochemistry, 2023
Heena Rehman, Md Iftekhar Ahmad
The shape of the coronavirus is variable from spherical, elliptical to pleomorphic form with the size of 125 nm as shown by cryo-electron tomography and cryo-electron microscopy (Neuman 2006, Bárcena et al. 2009). The characteristic feature of coronavirus is the presence of club or clove head-shaped spikes on the surface. The name of coronavirus is named after the presence of spikes (corona refers to the crown). Some of the common features of coronavirus are the presence of conserved genomic organisation with a large replicase gene preceded by structural and accessory genes; expression of non-structural genes by ribosomal frameshifting, several unique enzymatic activities encoded within replicase–transcriptase polyprotein, expression of the downstream gene by 3′ nested subgenomic messenger RNA (mRNA) (Strauss and Strauss 2008). The viral envelope is comprised of phospholipids, proteins and glycoproteins. The glycoprotein present on the surface of the envelope facilitates the identification and binding to the receptor. There are four proteins present on the surface of coronavirus, namely-spike (S), membrane (M), envelope (E), and haemagglutinin (HA) proteins (Figure 1).
Immunoinformatics-guided designing and in silico analysis of epitope-based polyvalent vaccines against multiple strains of human coronavirus (HCoV)
Published in Expert Review of Vaccines, 2022
Bishajit Sarkar, Md. Asad Ullah, Yusha Araf, Nafisa Nawal Islam, Umme Salma Zohora
Coronaviruses are a group of pathogenic viruses that mainly infect mammals and birds. These viruses cause diseases in the respiratory tract of humans, ranging from the common cold in otherwise healthy individuals to more serious and lethal conditions and even death [1,2]. The coronavirus family, also known as Coronaviridae, is the largest family of Nidovirales order. The coronavirus family consists of two subfamilies, Letovirinae and Orthocoronavirinae. Among these two subfamilies, the Orthocoronavirinae contains four genera, Alphacoronavirus, Betacoronavirus, Gammacoronavirus, and Deltacoronavirus. And among these four genera, the Alphacoronavirus and Betacoronavirus are known to cause diseases in humans [3]. Coronaviruses are enveloped viruses containing a positive-sense single stranded RNA genome. The genome of coronaviruses ranges from approximately 25 to 34 kb. The viral envelope comprises a lipid bilayer where the membrane (M) and spike (S) structural proteins are anchored [4,5].