Healthcare Providers and Virus Essay

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infection prevention and control theory, critically discuss the challenges of managing Hepatitis B in the community

One of the key public health issues that impacts innumerable individuals worldwide is viral hepatitis. This virus leads to substantial human mortality and morbidity from severe infection as well as chronic sequelae (including cirrhosis and chronic active hepatitis (with regard to hepatitis B, C & D). One among the ten commonest cancers that emerges across the globe -- hepatocellular carcinoma -- has been found to be linked closely to hepatitis B as well as, in some areas across the globe, to hepatitis C (Zuckerman., 2003).

HBV or Hepatitis B virus which belongs to the hepadna virus cluster is a double-stranded DNA virus that, atypically, gets reproduced via reverse transcription. HBV is endemic among humans and even hyper-endemic in several areas across the globe. Researchers have delineated various variants of the HBV virus. Natural infections by the hepadna virus are also found to occur in beechy ground squirrels, woodchucks, ducks, and other mammals. Initially, HBV was identified as the factor causing "serum hepatitis," which represents the commonest type of parenterally-transferred hepatitis viral infection, as well as a major factor contributing to lasting and severe liver infections. HBV's incubation period varies from1-6 months. Severe hepatitis infection's clinical characteristics are similar to other viral hepatitides' characteristics. Often, severe hepatitis B has been established as asymptomatic and anicteric. However, a serious case of jaundice may occur; also, severe liver failure might occur at times (Zuckerman., 2003).

Distinctive Properties

HBV is revealed to exist among five to ten percent of immune-competent adult humans, and in a shocking ninety percent (nine out of ten!) babies infected perinatally. Continued HBV carriage which is described as HBsAg's (HB surface antigen) presence within the blood serum for over half a year is predicted to impact roughly 350 million individuals across the globe. Its pathology is facilitated by the host's cellular immune responses to affected hepatocytes. Chronic, continuous replication of the virus can result in its evolution to cause hepatocellular carcinoma and cirrhosis (Zuckerman., 2003).

Within the foremost chronicity stage, the virus continually replicates within the liver. The viral genome's replicative intermediates can be discovered in DNA (Deoxyribonucleic acid) isolated from liver biopsy. HBV DNA, S1 proteins and HBeAg (the HB e antigen) which is a soluble antigen produced by HBV-infected hepatocytes, form the indicators of serum virus duplication. In case of individuals attacked and infected by the virus at a tender age, this stage can continue throughout life. However, more often, virus levels reduce with time. Ultimately, in case of most persons, immune clearance is obtained, of affected hepatocytes linked to sero-switching from HB e antigen to anti-HBe (Zuckerman., 2003).

In the duplication stage, the virus's genome might combine with some hepatocytes' chromosomal DNA; such cells can then persevere and increase clonally. Sero-switching into anti-HB seldom follows virus duplication clearance. Typically, HBsAg persevere in a second chronicity stage, owing to integrated viral DNA's expression (Zuckerman., 2003).

HBV-linked CTL (cytotoxic T. lymphocyte) response's antiviral and patho-genetic capacity has been corroborated through the surfacing of an acute necro-inflammatory liver ailment after adoptive transmission of HB surface antigen-specific CTL to an HBV transgenic mouse population. Strangely, CTLs also expel HBV replicative intermediaries from the human liver through secretion of type-1 inflammatory cytokines, thus, restricting transmission of the virus to unaffected cells as well as decreasing the amount of immunopathology needed for the purpose of infection termination (Chisari, Isogawa, & Wieland, 2011).

Continuing HBV infection has been marked by inadequate adaptive immune reactions, believed to stem from ineffective CD4+ T cell priming during the infection's initial phases and the resultant qualitatively and quantitatively weak CD8+ T cell reaction. Other factors which may play a part in virus persistence include immunological tolerance, T-cell receptor opposition, mutational epitope idleness, immunologically-privileged tissue infection and partial virus duplication down-regulation. But, the above pathways become clear only within the context of inefficient immune response. Thus, it makes up the disease's chief underlying cause in the community. Chronic infection has been marked by chronic injuries to liver cells, inflammation, regeneration, insertional cell-development control gene deregulation, and extensive DNA damage. These together give rise to hepatocellular carcinoma and liver cirrhosis in patients (Chisari, Isogawa, & Wieland, 2011).

Microbiology/Pathogenesis

HBV represents a 42-nanometer particle that consists of a nucleocapsid (electron-rich core), which has a diameter of 27 nanometers, enclosed by an external HBsAg covering imbedded in a membranous lipid originating from host cells.

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HBsAg is secreted in excessive quantities by affected hepatocytes as 22-nanometer tubular structures and particles (Zuckerman., 2003).

The aforementioned 22 nanometer units comprise of the dominant surface protein, both in glycosylated (gp 27) and non-glycosylated (p 24) form in roughly equimolar quantities, along with the secondary element -- the supposed middle proteins (i.e, gp 36 and gp 33) comprising of pre-S2 sphere, a glycosylated 55 amino acid N-terminal extension. HBV's surface composition is similar. The only difference is, it comprises of bulky surface proteins (gp 42 and p 39), including pre-S1 as well as pre-S2 areas. The above mentioned big surface proteins do not appear in circular 22 nanometer particles (however, they might exist in tubular kinds among highly viremic persons) and their identification in the blood serum is linked to viremia. The sphere that links to a particular hepatocyte HBV receptor is deemed to be located in the pre-S1 area (Zuckerman., 2003).

HB virion's nucleocapsid constitutes its virus genome encircled by a key antigen (HBcAg). This genome that has an approximate length of 3.2 kilobases possesses a curious structure and comprises of a couple of linear DNA strands maintained through base-pairing at 5' ends in a spherical arrangement. One strand is incomplete. The 3' extremity is linked to a DNA polymerase particle that can complete the strand if provided with de-oxy-nucleoside triphosphates (Zuckerman., 2003).

Organization of the HBV Genome

Over 12 HBV isolates' genomes have been duplicated in order to ascertain the entire nucleotide sequence. Genome coding capacity examination shows 4 ORFs (open reading frames) retained between the isolates (Zuckerman., 2003).

Of the above 4 ORFs, the first encodes the many surface protein variants and comprises of 3 in-frame methionine codons employed in the translation commencement process. Another promoter can be found upstream of pre-S1 commencement codon, which guides the creation of a 2.4-kb Messenger RNA (ribonucleic acid) co-terminal with different surface messages. It is decoded to generate big surface proteins (pre-S1) (Zuckerman., 2003).

Further, the key ORF possesses a couple of in-stage commencement codons. This "precore" area is well-preserved, possesses a signal sequence's attributes, and is in charge of HBeAg production (Zuckerman., 2003).

Another ORF, which makes up the biggest and overlays the remaining 3 ORFs, translates the virus polymerase. This seems to be like an alternative translation outcome of the 3.5kb RNA, seemingly produced subsequent to the ribosome's internal initiation.

Researchers believe the amino-terminal sphere acts as protein primer in case of minus-strand development. Further, a spacer area exists, followed by DNA polymerase which is DNA and RNA-dependent (Zuckerman., 2003).

The last ORF has been labeled "x" as its tiny gene product's function was unknown. But, "x" is now proven by scholars to constitute a transcriptional transactivator (Zuckerman., 2003).

Viral Variants and Pathogenesis of Infection

There has been growing evidence of the relationship of particular HBV mutants and distinctive clinical manifestations; these can impact the disease's typical course and give rise to antiviral agent resistance (Baumert& Blum, 2000; Baumert, Barth & Blum, 2005; Zoulim, 2004; Pawlotsky, 2005). Natural mutations within several genotypes are determined in both non-structural and structural genes, and regulatory viral components. The pre-C (precore) stop codon transformations which lead to HBeAg loss represent the best described mutants (Liang, Hasgawa, Rimon, Wands, Ben-Porath, 1991). Baumert, Rogers, Hasegawa & Liang, (1996), Baumert and colleagues (2005), Buckwold and colleagues (1996), and Schildgen and colleagues (2006) identified mutation groups within the main promoter, leading to enhanced virus duplication, as well-described. Lastly, Zoulim (2004), Pawlotsky (2005), Liang, Hasgawa, Rimon, Wands, and Ben-Porath (1991), Baumert, Rogers, Hasegawa & Liang (1996), Baumert and colleagues (2005), Buckwold and colleagues (1996), Schildgen and colleagues (2006), and Kann and Gerlich (2005) adequately described transformations in reverse polymerase/transcriptase genes that resist antivirals. Moreover, a number of HB virus surface gene changes have been detected, changing HBsAg's antigenicity and viral covering structure (Baumert, Barth & Blum, 2005; Zoulim, 2004; Pawlotsky, 2005; Liang, Hasgawa, Rimon, Wands, Ben-Porath, 1991; Baumert, Rogers, Hasegawa & Liang, 1996; Baumert, et al., 2005; Buckwold et al., 1996; Schildgen et al., 2006; Kann, & Gerlich, 2005).

Standard Precautions

Accepted precautions integrate key aspects of BSI (body substance isolation) and UP (universal precautions), and are grounded in the premise that every body fluid, secretion, blood, excretions (with the exception of sweat), mucous membranes and broken skin can contain communicable.....

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