Viral pathogenesis

In addition to the role of chemokines/chemokine receptors in viral infection, transmission, and pathogenesis, chemokines also play important roles in cellular trafficking and survival pathways. The role of chemokines and their receptors are of particular importance in the development of neurologic complications of AIDS, involving mechanisms discussed in the following sections. 

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). 

Viral hepatitis can occur at any age and is the most common cause of liver disease in the world. The true prevalence and incidence may be underreported because most patients are asymptomatic. The epidemiology, etiology, and pathogenesis vary depending on the type of hepatitis and will be considered separately below. 

Fantuzzi L, Belardelli F, Gessani S. Monocyte/macrophage-derived CC chemokines and their modulation by HIV-1 and cytokines a complex network of interactions influencing viral replication and AIDS pathogenesis. J Leukoc Biol 2003 74(5) 719-725. 

Because of their interference with the interaction between the viral envelope gpl20 glycoprotein and the cellular CD4 receptor, poly anionic substances not only inhibit virus adsorption to the cells but also block syncytium (giant cell) formation between the HIV-infected (gpl20 + ) cells and uninfected (CD4 + ) cells. Since syncytium formation results in a selective destruction of the CD4+ cells, this syncytium formation may play an important role in the pathogenesis of AIDS (a hallmark of which is a progressive decline of the CD4+ cells). 

Despite the protective effect of NO against various viral infections, workers in several studies have shown a harmful role of NO in many systems. NO seems to play a part in the development of pneumonia caused by influenza virus [128], in the pathogenesis in mice of tick-borne encephalitis flavivirus infection [131], and in worsening the course of the murine myocarditis caused by coxsackievirus B3 [132]. In addition, pneumonia in mice induced by herpes simplex virus type 1 could be suppressed by the inhibitor of iNOS [133]. The issue of whether NO acts as an inhibitor of viral replication or as a harmful agent, therefore, remains unanswered. This issue is particularly evident in HIV-1 infection, since NO seems to act as a double-edged sword in the pathogenesis of HIV-1. 

Persistent, high-level viral replication is now established as the motivating factor of HIV pathogenesis with about 10 billion virions (viral particles complete with RNA and envelope) in an infected person daily. 

Medicinal thrombocytopenia can emerge under the use of different medicines, including interferon. The main mechanism of medicinal thrombocytopenia pathogenesis is assisted by the destruction of thrombocytes by the complement which is activated during antibody preparation. On withdrawal, the content of thrombocytes in blood is normalized. The formation of antibodies to thrombocytes in patients with viral hepatitis C occurs due to the destruction of membrane glycoproteins by the viruses. 

There is much more to this functional complexity than we have been able to discuss in this review. For instance, we have not touched on the complex intranuclear network mediated by the nuclear lamins, which is critically important for human health as reflected in the numerous disease phenotypes that are emerging due to mutation in lamins and their associated protein partners. We have also not discussed the association of IFs with molecules involved in bacterial and viral pathogenesis, such as the Ebstein-Barr virus latent infection membrane protein (LMP) (Liebowitz et al., 1987) or viral kinases such as the herpes simplex virus US3 kinase (Murata et at, 2002) that may be important in remodeling IFs during infection. It is clear, however, from the many critical cellular functions we have discussed in this review, that the IF structural and signaling scaffold is involved in wide-ranging functions that are important for fundamental... 

Influenza virus sialidase poses a highly attractive target for antiviral drug design due to its prominent position at the surface of the virion and its profound role in viral pathogenesis. Random screening programs identified a number of... 

Viral infection is a possible triggering factor. Various viruses are known to be associated with SLE, including myxoviruses, reoviruses, measles, and rubella (A22). The pathogenesis of UVR and viruses in generating autoantibodies will be discussed in a later section. 

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