Macrophages play a crucial role in respiratory viral infections. However, the mechanisms by which these cells are recruited locally are not fully understood. The current authors studied the role of the chemokines monocyte chemotactic protein (MCP)-1, -2, -3 and -4 on monocyte/macrophage recruitment during respiratory viral infections. Levels of these chemokines were investigated in nasal aspirates from 6-12-yr-old children suffering from respiratory viral infections, caused by rhinoviruses, influenza viruses, parainfluenza viruses, adenoviruses and respiratory syncytial virus.MCP-3 and -4 were significantly higher in samples derived from virus-infected children compared with samples from the same children when they had been asymptomatic. Concentrations of both chemokines were found to significantly correlate with the number of recruited nasal macrophages. Chemotaxis assays showed that purified MCP-3 and -4 from nasal aspirates showed biological activity in vitro. There were no significant differences in MCP-1 and -2 levels between both groups.The present data indicates that monocyte chemotactic protein-3 and -4 may have an important role in macrophage recruitment in children with proven upper respiratory viral infections. These chemokines could be potential targets for therapeutic intervention in respiratory viral infections.
The term pathogenesis refers to the processes or mechanisms to generate an injury or illness, in this case induced by a viral infection. The results of a viral infection depend on factors related to the nature of the virus, the host and the environment. They include number of infectious particles, the way to reach the target tissue, the rate of multiplication, the effect of virus on cell functions and the host's immune response. Three requirements must be satisfied to ensure the infection of an individual host [ ]• Sufficient virus must be available to initiate infection,• Cells at the site of infection must be accessible, susceptible, and permissive for the virus• Local host anti-viral defense systems must be absent or initially ineffective.To infect its host, a virus must first enter cells at a body surface. Common sites of entry include the mucosal linings of the respiratory, alimentary and urogenital tracts, the outer surface of the eye conjunctival membranes or cornea , and the skin."mong the factors that affect the infection process are . Virus-dependent factors. They usually are dependent on the virus structure. a. Virulence. Virulence is under polygenic control and is not assignable to any isolated property of the virus, but is often associated to characteristics that favor viral replication and cellular injury. For example, virulent viruses multiply themselves readily at high temperatures prevailing during the disease, block the synthesis of interferon and macromolecules related to immune system. Viral virulence is a quantitative statement of the degree or extent of pathogenesis. In general, a virulent virus causes significant disease, whereas an avirulent or attenuated virus causes no or reduced disease, respectively.b. Measuring Viral Virulence. Virulence can be quantified in a number of different ways. One approach is to determine the concentration of virus that causes death or disease in % of the infected organisms. This parameter is called the % lethal dose LD , the % paralytic dose PD , or the % infectious dose ID , depending on the parameter that is measured. Other measurements of virulence include mean time to death or appearance of symptoms, as well as the measurement of fever or weight loss. Virus-induced tissue damage can be measured directly by examining histological sections or blood samples. For example, safety of live attenuated poliovirus vaccine is determined by assessing the extent of pathological lesions in the central nervous system in experimentally inoculated monkeys. Indirect measures of virulence include assays for liver enzymes alanine or aspartate amino-transferases that are released into the blood as a result of virus-induced liver damage [ ].
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