Viral infections preventing recurrent

Qll Acute exacerbations of chronic bronchitis can be caused either by viral or bacterial infections. Production of thick, green sputum suggests Chandra has a bacterial infection. Common bacterial pathogens affecting the lung include Streptococcus pneumoniae and Haemophilus influenzae. It is recommended that COPD patients receive influenza vaccine each year pneumoccocal vaccine is also often recommended in chronic lung disease and may prevent recurrence of chest infection in the elderly. 

The antiviral mechanism of action of acyclovir has been reviewed (72). Acyclovir is converted to the monophosphate in herpes vims-infected cells (but only to a limited extent in uninfected cells) by viral-induced thymidine kinase. It is then further phosphorylated by host cell guanosine monophosphate (GMP) kinase to acyclovir diphosphate [66341 -17-1], which in turn is phosphorylated to the triphosphate by unidentified cellular en2ymes. Acyclovir triphosphate [66341 -18-2] inhibits HSV-1 viral DNA polymerase but not cellular DNA polymerase. As a result, acyclovir is 300 to 3000 times more toxic to herpes vimses in an HSV-infected cell than to the cell itself. Studies have shown that a once-daily dose of acyclovir is effective in prevention of recurrent HSV-2 genital herpes (1). HCMV, on the other hand, is relatively uninhibited by acyclovir. 

Trifluridine (trifluorothymidine) is a fluorinated pyrimidine nucleoside that inhibits viral DNA synthesis in HSV-1, HSV-2, CMV, vaccinia, and some adenoviruses. It is phosphorylated intracellularly by host cell enzymes, and then competes with thymidine triphosphate for incorporation by the viral DNA polymerase (Figure 49-3). Incorporation of trifluridine triphosphate into both viral and host DNA prevents its systemic use. Application of a 1% solution is effective in treating keratoconjunctivitis and recurrent epithelial keratitis due to HSV-1 or HSV-2. Cutaneous application of trifluridine solution, alone or in combination with interferon alfo, has been used successfully in the treatment of acyclovir-resistant HSV infections. 

In this particular instance the drug aid inside an infected cell to get converted into a triphosphate , which is subsequently incorporated directly into DNA. In fact, this phenomenon terminates elongation of the DNA, and thereby prevents viral replication mechanism significantly. It fails to eradicate latent herpes. It is observed to be unpredictable to a certain extent as a topical prophylactic agent against particularly the recurrent infections caused by HSV-1 and HSV-2. 

---