As an HIV pathogen, I would be one of the microbial pathogens that have no cure. The HIV cell divides rapidly ones it has established itself inside a human cell. The high speed of replication enables the virus to attack and infect other cells in the human body quickly. As an HIV pathogen, I would have all the necessary structures in place that would help me infect specific human body cells. As a microbe, I must have features that would enable me to live and survive in my habitat or environment ( Wissing, Galloway & Greene, 2010).
As an HIV microbe, I must be able to obtain a phospholipid envelope from the human cell membrane which will protect and coat my inner cell structure. On the phospholipid membrane, I must also have the necessary glycoproteins for my attachment onto the appropriate human cells. I must have in place the three critical enzymes; the reverse transcriptase, integrase, and the protease enzyme. All the three enzymes play important roles and are responsible for the survival and replication of the virus. I would use the reverse transcriptase to reverse-transcribe my RNA genome into a DNA genome during cell replication inside a human cell. Without this process, I would not be able to replicate. The integrase enzyme would, in turn, be used to integrate my new DNA strand onto the human DNA ( Briggs, et al. 2009) . The protease would then cut down the complex proteins into smaller classified proteins ( Sundquist & Kräusslich, 2012) .
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As an HIV virus, I would have all the necessary features to be able to survive in the human body cells. I would have a phospholipid envelope to help protect my inner cell structure in the blood stream, for example. I would be sure to develop and contain the essential glycoproteins in order to attach to the intended human cells such as the CD4positive cells. These glycoproteins will also help me initiate infection ( Mayer & Venkatesh, 2011) .
References
Wissing, S., Galloway, N. L., & Greene, W. C. (2010). HIV-1 Vif versus the APOBEC3 cytidine deaminases: an intracellular duel between pathogen and host restriction factors. Molecular aspects of medicine , 31 (5), 383-397.
Mayer, K. H., & Venkatesh, K. K. (2011). Interactions of HIV, other sexually transmitted diseases, and genital tract inflammation facilitating local pathogen transmission and acquisition. American Journal of Reproductive Immunology , 65 (3), 308-316.
Briggs, J. A., Riches, J. D., Glass, B., Bartonova, V., Zanetti, G., & Kräusslich, H. G. (2009). Structure and assembly of immature HIV. Proceedings of the National Academy of Sciences , 106 (27), 11090-11095.
Sundquist, W. I., & Kräusslich, H. G. (2012). HIV-1 assembly, budding, and maturation. Cold Spring Harbor perspectives in medicine , 2 (7), a006924.
