A virus can be compared to an intruder or a thief, and that is because viruses are not cells (Mateu, 2013) They do not really need a nucleus and they would not need a cytoplasm or a membrane to protect them (ScienceDaily, 2019,). Viruses are not formed in the same way most cells are. Viruses mostly break inside a host cell for the purpose of using the hosts cell’s enzymes and organelles which the virus requires in order to reproduce (De Robertis, Nowinski and Saez, 1970). Therefore, a virus can be known as an intracellular parasite (Dimmock, Easton and Leppard, 2001) Since viruses are not formed in the same way most cells are, a virus can only reproduce by invading a host cell where their genome is a material of nucleic acid that can be DNA or RNA (Gelderblom, 2019) which goes onto to reproduce internally within living cells in a process known as viral replication (Hammer, 2019) and have the adaption of their biological system, which can transport the synthesis that belongs to specialized particles known as the virion, which itself houses the viral genome (Knipe and Howley, 2013, Fields of virology), and then directs it towards many cells within the body. This then increases their pathogenic outcome of transmission (Nathanson, 1997, Viral Pathogenesis) as the virus is able to spread their genome sequence from an infected host to another that is unaffected (Tennant, Fermin and Foster, n.d.). Carp may be the most prized fish species in the world, due to the various varieties of carp that are widely available, becoming a highly regarded fish by many people, who pay large sums of money for them. However, these valuable carp often become diseased. This report will look at cellular processes in carp and how they relate to pathogens. However, it will not look at treatments for carp diseases.
One of the biggest pathogenic killers is spring carp viremia virus (SVCV) (see plate 1) a cytopathic virus that is related to the Rhabdoviridae family (Ashraf U, 2019) a variation of vesiculovirus that causes febrile systemic infection affecting a large quantity of cyprid species (MacLachlan and Dubovi, 2017) SVCV is common within the regions of Europe and can be found within serval other regions that includes United states and China (Fowler and Miller, 2008) SVCV pandemics have been reported to cause some serious losses to the carp population (Cmsadmin.atp.co.il, 2019) Common carp are much more vulnerable of getting the deadly disease (Oie.int, 2019) which mostly affects the fish throughout springtime. The possible explanation for this would be because, average water temperatures during those months are generally between 100c to 170c. This is the perfect temperature for SVCV to prosper (Ahne , 2002). However, if the temperature of the water is higher, carp carrying the virus begin to produce immune response antigens, which help combat the SVCV. The antigens then make the fish immune to the SVCV (Microbiologyresearch.org, n.d) Carp pick up the virus from actually eating the faeces and urine made by fish carrying the virus. However, in the carp’s environment there will be blood sucking leeches as well as the carp louse which are parasites that too are carries of the SVCV coming under the category of mechanical vector (In.gov, n.d))
The SVCV pathogen can be known when examined under a microscope, due to its distinguishable rod and otherwise bullet shaped attribute (Atrium.lib.uoguelph.ca, 2019). Every strand of SVCV houses a negative strand of RNA genome (Mahy and Van Regenmortel, 2014). On the other hand, the sequencing RNA ultimately requires instructions to construct the five proteins nucleoprotein, phosphoprotein, matrix protein, glycoprotein and the large polymerase protein (Lenoir, 1973) The five proteins are required for the transference of the SVCV, as the virus uses the proteins as hosts in order to affect healthy unaffected cells (Wei et al., 2016). It then uses the infested protein to spread from one place to another within the body. The SVCV virus is restricted to a certain quantity of hosts cells. The virus can do this by acting as a lock and key fit that wedges amongst the proteins on the outside of the virus and then the receptor molecules on the host’s surface (De Robertis, Nowinski and Saez, 1970). Only the nucleoprotein is connected to viral RNA, which helps in the configuration of nucleocapsid shaping and virus assembly morphing. The matrix protein collects pathogen and it then has the ability to alternate the pathogens structure (Zhang et al., 2009). Glycoprotein is a part of viral endocytosis (Vogt et al., 2005).The SVCV G protein, a viral protein present on the gene encoding surface has the power to design trimeric peplomers and activates cellular signalling pathways which goes onto beginning the process of viral endocytosis making SVCV G protein the central point of vigilant counteracting antibodies. (Sorkin and von Zastrow, 2010). Endocytosis is a form of active transport that shifts molecules like organelles, cell pieces and even other whole cells into a different individual cell (Marsh, 2001).
Plate 1 SVCV Diseased carp (Fishelp, n.d)
Endocytosis appears in many different variations; however, all share a common similarity to the cell’s plasma bilayer, by developing a pocket around all of the target particles (Kubo et al., 2012). Once the pocket has successfully wrapped itself around the developing pocket, the pocket then pinches off leaving behind just one molecule which then gets encapsulated within a newly assembled intracellular membrane. This is known as pinocytosis (La Bella, 1973). Alternatively, there is the opposite process, where materials get placed inside a cell. This process is known as exocytosis (Regazzi, 2011). Material gets dislodged from the cell moving towards the extracellular fluid where the waste material gets enfolded within a membrane that then fuses in the inside of the plasma membrane (Gauthier et al., 2011).The whole fusion process causes the membrane envelope to unlock from the outside of the cell, which then causes the waste material to get ejected directly into the extracellular space.
For SVCV to colonize by spreading from one cell to the next, duplicating as it goes, which increases the variety of the virus. SVCV needs to take over the active site. The virus has one obstacle that prevents it from taking over the active site. IFN referred to as an interferon are proteins produced by cells when endanger from being taken over from viral infection (GC, 2009). Interferons are part of the non-specific immune system that only become active when being stimulated to a response (Le Page C, 2000) The main function of an interferon is to tamper with any intracellular pathogen that chooses to intrude a host cell which the virus causes the host cell to produce antiviral response.
Cells which have been invaded by the SVCV will be recognized by the immune response, which act’s on trying to prevent SVCV from replicating inside one cell then transferring to the next by using a biological process known as phagocytosis (Naik, 2013). A cellular process that is crucial for the removal of pathogens. It does this by engulfing of solid particles performed by the cell membrane, which then gets broken down by enzymes and then absorbed by cells (Gordon, 1999). Phagocytosis is a key stage used for the removal of pathogens and cell debris. On the other hand, SVCV has evolved a tactic to defeat interferon response. SVCV does this by invading a host cell in response to the invasion of SVCV. The invaded cell will send out a signal known as the retinotic acid enzyme inhibitor, which can be termed RIG-1 (Matsumiya, 2011). This gene acts as another line of defence to safeguard the cell by acknowledging harmful viruses only after the virus itself has been located. A immediate response will be sent out which effectively activates for the production of interferons produced from the immune response (Finter, 1967).
Fish that are unfortunate enough to have the virus will demonstrate signs such as petechial haemorrhage causing a serious problem towards the skin, gills, eyes and most vital organs. In addition, other negative consequences of SVCV usually involve gill deterioration, inflamed and solid hard spleen, hepatic necrosis enteritis and pericarditis (Aphis, 2004)
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