The Mechanisms Adenovirus Uses to Ensure Life Cycle (Research Paper Sample)

The Mechanisms Adenovirus Uses to Ensure Life Cycle
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The Mechanisms Adenovirus Uses to Ensure Life Cycle
Adenovirus has mechanisms that adapt it to surviving in the host cell in order to ensure the progression of its life cycle. The most important mechanisms employed by adenovirus utilize the host cell motor proteins and the cytoskeleton to perpetrate its life cycle. Host cell uptakes adenovirus into the endocytic vesicles through a receptor mediated process, and the virus moves from the endosome (Engelke, Burckhardt, Morf, and Greber, 2011). Several studies suggest that as opposed to organelles or transport vesicles, the adenovirus binds directly to the minus end-directed motor dynein of the microtubules for transport to the nucleus which promotes infection. This assertion that motor proteins, cytoskeleton, and other host cell proteins such as dynein have a role in adenovirus infectivity and ensuring its life cycle is the justification for this study (Scherer and Vallee, 2011). The paper discusses the mechanisms by which adenovirus employs the motor proteins and host cell cytoskeleton to ensure its life cycle.
The host cell is indispensable for the survival of adenovirus by offering extensive support to the virus from entering the cell by the use of receptors, endocytic pathways and signalling mechanisms, movement into the cytosol by membrane disruption because the adenovirus is non-enveloped but encapsidate an approximately 36kbp double stranded DNA genome, and transported to the nucleus by microtubules made of dynein/dynactin motor complex (Engelke, Burckhardt, Morf, and Greber, 2011). These motor proteins are essential for the life cycle of adenovirus because they enable the virus to move to the host cell nucleus for genome replication. This enables the host cell to play key roles for the virus such as RNA splicing, alteration of chaperone mediated protein which is folding with 100k folding factor and viral hexon protein, and antigen presentation by class I major histocompatibility complex (Scherer and Vallee, 2011). This mechanism provides a useful interaction in using adenovirus as a vehicle for gene delivery in therapy or eradicating neoplastic cells.
The association between viral and host proteins secure the stability of the virus within the host cell. The mechanism is essential for adenovirus adhesion to cell receptors, and binding to penton base enabling integrins to facilitate the dynamin dependent endocytosis which is responsible for anchoring adenovirus to the cytoskeleton fibres. The internal protein IV, on the other hand, is employed in enabling the virus to escape from endosome into the cytosol where it is uncoated, releases internal proteins for cementing, and sheds virion fibres (Scherer and Vallee, 2011). The virion particle translocates to the nucleaus through cytoskeleton microtubules and motor proteins in a bidirectional mode of transport. The adhesion proteins form a nuclear-pore complex that allows the subviral particles to attach to the nuclear envelope and release its viral DNA material into the nucleus for replication. In this mechanism by which subviral particles get to the nuclear pore complex and inject genomic material into the nuclear, adenovirus uses dynein cofactor dynactin existing as a microtubule cytoskeleton dependent transport (Engelke, Burckhardt, Morf, and Greber, 2011). It is, therefore, evident that intact microtubules are indispensable for adenovirus particles to move in bidirectional in the host cell while dynactin promotes long, periphery directed, and fact centre viral motion both of which are essential in viral replication, infection, and perpetuating its life cycle.
Recruiting dynein through an evolutionary novel mechanism that uses pH primed hexon for direct binding of adenovirus indicates how the virus uses motor proteins for infection, replication, and continuity of its life cycle (Engelke, Burckhardt, Morf, and Greber, 2011). This information is vital in understanding the relationship between physiologic cargo and pathogenic recruitment as an evolutionary mechanism of dynein mediated transport of adenovirus to the nuclear in order to ensure its life cycle. Further evidence suggests that microtubules are necessary for the transport of the virus due to the observed linear trajectory movements which are consistent with the arrangement of microtubules. Host cell cytoskeleton and motor proteins are prerequisites for the life cycle of adenovirus because, when nocodazole is used to depolymerize microtubules in host cells infected with adenovirus, the infection reduces because the redistribution and transport of the viral particles to the nuclear for replication is inhibited (Scherer and Vallee, 2011). The closer association between the virus and dynein, as well as the role of host cell microtubule motors in regard to intracellular adenovirus transport, ensures the life cycle of the virus.
Finally, adenovirus depends on utilising host cell cytoskeleton, and motor proteins in ensuring its life cycle continue as evidenced in this discussion. The cytoplasmic dynein mediated motility of adenovirus utilises motor proteins such as penton base, hexon, fibre, and proteins IIIa, VI, VIII, and IX, which support viral endosomal escape, binding of the naked capsid adenovirus to dynein, dismantling the virus, and delivering viral DNA material into the host cell nuclear for replication aimed at producing viruses (Engelke, Burckhardt, Morf, and Greber, 2011). These proteins are sensitive to the cytosolic pH resulting in changes, in the hexon and adenovirus capsid which are pH dependent biochemical characteristics. The replication and life cycle of adenovirus are affected by changes in the intracellular pH which is a crucial observation in confirming the fundamental role played by motor proteins and host cell cytoskeleton in ensuring the life cycle of adenovirus. This is further supported by the findings identifying the interaction between the cytoplasmic dynein subunit and hexon, involvement of regulators specific to cytoplasmic dynein...