Viruses viral infections

Viruses (from the Latin virus referring to poison) are nonliving obligate intracellular parasites composed of protein and nucleic acid (DNA or RNA) that manipulate the host cell to produce and manufacture more viruses. Viral infection occurs by tire attachment of virus particles to specific cell receptors within the host cell. After fusion of the host cell plasma membrane with the virus outer envelope, the protein-based viral nucleocapsid (containing the viral DNA) is transported to the host cell nucleus, where components of the viral particle inhibit macromolecular synthesis by tire host cell. Herpes viral DNA and new viral nucleocapsid synthesis occurs within the host nucleus, with the acquisition of new viral envelopes via a budding process through the inner membrane of the host nucleus. The mature newly synthesized viral particles are subsequently... 

Interferons [alFN, piFN and ylFN]. Interferons are a family of glycosylated proteins and are cytokines which are produced a few hours after cells have been infected with a virus. Interferons protect cells from viral infections and have antiviral activities at very low concentrations ( 3 x 10 M, less than 50 molecules are apparently sufficient to protect a single cell). Double stranded RNA are very efficient inducers of IFNs. There are three main types of IFNs. The aIFNs are synthesised in lymphocytes and the piFNs are formed in infected fibroblasts. The a and P families are fairly similar consisting of ca 166 to 169 amino acids. Although ylFNs are also small glycosylated proteins (ca 146 amino acids), they are different because they are not synthesised after viral infections but are produced by lymphocytes when stimulated by mitogens (agents that induced cell division). 

Interferons (EFNs) are a family of multifunctional secreted proteins in vertebrates. Their most prominent functions are their antiviral properties on homologous cells against a wide range of viruses. It is important to note that prior exposure to EFN is required to render cells resistant to viral infection and replication. In contrast to antibodies, EFNs have no direct neutralizing effect on viruses. 

HSV2 (herpes simplex virus 2), which causes significant morbidity and is an important cofactor for the transmission of HIV infection was recently targeted in a mouse model by local application of siRNA mixed with lipids. The results suggested that siRNA could work as active components of microbicides to prevent viral infection or transmission [2]. 

Before therapy is begun, culture and sensitivity tests (see Chap. 7) are performed to determine which antibiotic will best control the infection. These drug are of no value in the treatment of infections caused by a virus or fungus. There may be times when a secondary bacterial infection has occurred or potentially will occur when the patient has a fungal or viral infection. The primary health care provider may then order one of die... 

M ore than 200 viruses have been identified as capable of producing disease Acute viruses, such as the common cold, have a rapid onset and quick recovery. Chronic viral infections, such as acquired immunodeficiency syndrome (AIDS), have recurrent episodes of exacerbations (increases in severity of symptoms of the disease) and remissions (periods of partial or complete disappearance of the signs and symptoms). Display 14-1 describes the viruses discussed in this chapter. 

Although infections caused by a virus are common, antiviral drugp have limited use because they are effective against only a small number of specific viral infections. 

CMV, a virus of the herpes family, isa common viral infection. Healthy individuals may beoome infected yet have no symptoms. However, immunocompromised patients (such as those with HIV or cancer) may have the infection. Symptoms include malaise, fever, pneumonia, and super infection. Infants may acquire the virus from the mother while in the uterus, resulting in learning disabilities and mental retardation. CM V can infect the eye, causing retinitis. Symptoms of CMV retinitis are blurred vision and decreased visual acuity. Visual impairment is irreversible and can lead to blindness if untreated. 

Bacterial and viral myositis is well recognized as a clinical entity by muscle pathologists. The viruses most commonly involved appear to be the Coxsackie viruses, the arboviruses, influenza virus, and HIV, but the mechanism whereby the viral infection gives rise to the myositic syndrome is not known. A detailed discussion of such problems is presented later on pages 333-334. 

Abstract In 2007, the world celebrated the 50th anniversary of the discovery of interferon (IFN) by Isaacs and Lindemnann. Subsequently, the IFN-a gene was cloned, fully sequenced and IFN-a was produced in recombinant form. Recombinant IFN-a is now used as the basis for treatment of chronic hepatitis C virus infection and can also be used to treat certain forms of chronic hepatitis B virus infections. IFNs have also been used in other viral infections, although with less success. The antiviral mechanisms of IFNs are reviewed in this chapter as well as the utility of IFNs in the treatment of persistent viral infections. 

In pharmacology, two adamantane derivatives. Amantadine (1-adamanta-neamine hydrochloride) and Rimantadine (a-methyl-1-adamantane methyla-mine hydrochloride) (see Fig. 24), have been well known because of their antiviral activity [129]. The main application of these drugs is prophylaxis (treatment to prevent the onset of a particular disease) and treatment of influenza-A viral infections. They are also used in the treatment of parkinsonism and inhibition of hepatitis-C virus. Memantine (1-amino-3,5-dimethyladaman-tane) (see Fig. 24) has been reported effective in slowing the progression of Alzheimer s disease [130]. 

The natural killer cells (NK) are the host s primary innate immune responders against viral infections. Studies have shown morphine to suppress the cytolytic activity of NK cells (Shavit et al. 2004). In vivo studies carried out in the Indian rhesus macaques looked at chronic morphine administration and SIV the equivalent of HIV in apes. This group concluded that morphine contributed to the pathogenesis of Simian Immunodeficiency Virus (SIV) infection and that this contribution occurred in conjunction with the replication of viral proteins including Tat (Noel and Kumar 2006 Noel et al. 2006). 

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