Russian Health Ministry registers world’s first nasal spray coronavirus vaccine – World – TASS

MOSCOW, April 1. /TASS/. The world’s first nasal spray coronavirus vaccine has been registered in Russia, the Health Ministry said in a statement on Friday.

“The Russian Health Ministry has registered the nasal spray form of the Gam-COVID-Vac (Sputnik V) coronavirus vaccine developed by the Health Ministry’s Gamaleya Research Institute of Epidemiology and Microbiology,” the statement reads.

According to the ministry, the vaccine consists of two components based on the type 16 and type 5 adenovirus vectors. The two doses will be administered with an interval of three weeks.

This kind of vaccination creates mucosal immunity against the coronavirus within the respiratory tract. “The use of a nasal spray induces a humoral immune response (boosting IgA antibody titers in the blood and nasal secretions and virus-neutralizing IgG antibody titers in the blood) and a cellular immune response to the infection caused by SARS-CoV-2,” the statement added.

At this point, the vaccine is intended for the immunization of individuals over the age of 18.

Russian Health Minister Mikhail Murashko said earlier that the use of the nasal spray coronavirus vaccine would be included in recommendations for booster shots.

This type of Vaccine uses Adenoviruses (mRNA) DNA Replication

Replication Edit
Adenoviruses possess a linear dsDNA genome and are able to replicate in the nucleus of vertebrate cells using the host’s replication machinery.[2] Entry of adenoviruses into the host cell involves two sets of interactions between the virus and the host cell.[2] Most of the action occurs at the vertices. Entry into the host cell is initiated by the knob domain of the fiber protein binding to the cell receptor.[2] The two currently established receptors are: CD46 for the group B human adenovirus serotypes and the coxsackievirus/adenovirus receptor (CAR) for all other serotypes.[2] There are some reports suggesting MHC molecules and sialic acid residues functioning in this capacity as well. This is followed by a secondary interaction, where a motif in the penton base protein (see capsomere) interacts with an integrin molecule. It is the co-receptor interaction that stimulates entry of the adenovirus. This co-receptor molecule is αV integrin. Binding to αv integrin results in endocytosis of the virus particle via clathrin-coated pits. Attachment to αV integrin stimulates cell signaling and thus induces actin polymerization, which facilitates clathrin-mediated endocytosis, and results in virion’s entry into the host cell within an endosome.[16]

Once the virus has successfully gained entry into the host cell, the endosome acidifies, which alters virus topology by causing capsid components to disband. The capsid is destabilized and protein VI, which is one of the capsid constituents (see Adenovirus genome) is released from it.[17] These changes, as well as the toxic nature of the pentons, destroy the endosome, resulting in the movement of the virion into the cytoplasm.[2] With the help of cellular microtubules, the virus is transported to the nuclear pore complex, whereby the adenovirus particle disassembles. Viral DNA is subsequently released, which can enter the nucleus via the nuclear pore.[18] After this the DNA associates with histone molecules already present in the nucleus, which allows it to interact with the host cell transcription machinery[citation needed]. Then, viral gene expression can occur, without integrating the viral genome into host cell chromosomes,[19] and new virus particles can be generated.

The adenovirus life cycle is separated by the DNA replication process into two phases: an early and a late phase.[2] In both phases, a primary transcript that is alternatively spliced to generate monocistronic mRNAs compatible with the host’s ribosome is generated, allowing for the products to be translated.

The early genes are responsible for expressing mainly non-structural, regulatory proteins.[2] The goal of these proteins is threefold: to alter the expression of host proteins that are necessary for DNA synthesis; to activate other virus genes (such as the virus-encoded DNA polymerase); and to avoid premature death of the infected cell by the host-immune defenses (blockage of apoptosis, blockage of interferon activity, and blockage of MHC class I translocation and expression).

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