RETROVIRUSES and AIDS
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Retroviruses and Aids
Introduction
A virus is a tiny microbe that can infect a cell in the body of a human being. When the virus enters the cell, it uses a cellular component to replicate. The classification of the viruses differs in several ways. They include; the kind of genetic materials used, for instance, DNA or RNA, the method they use to replicate, and their shape or structural features (Trysteen et al., p 314).
Retrovirus is one among the family viral known as retroviridae. RNA is mostly used as genetic material. Viruses and retroviruses appear different from each other in that their process of replication in the host cells is quite different. When the RNA invades the DNA of the host cell, it changes its genome. When it enters the host cell’s cytoplasm, the virus uses its transcriptase enzyme to produce DNA from the genome of its RNA. The currently new DNA is then maintained in the host cell genome by an integrase enzyme; at this point, the retroviral DNA is now called pro-virus. The host cell treats the new viral DNA as its genome, thereby translating the viral genes and the cell’s genes, producing the proteins required to mobilize new viral copies. Several enzymes help replicate the viruses (Gifford et al., p. 317). They include reverse transcriptase enzymes; these are the enzymes that change the RNA into the HIV DNA in the human being’s body.
Integrate enzyme; these enzymes combine the HIV DNA with the CD4 count cell’s DNA. Protease enzyme; these are the enzymes that cut short the HIV proteins’ long-chain into smaller pieces. Retroviruses have mainly three groups which have different subfamilies. They include; Oncoretroviruses (oncogenic retroviruses), spumaviruses (foamy viruses), and lentiviruses (slow retroviruses). The oncoretroviruses cause cancer in some species (Rumlova et al., p. 274). Also, lentiviruses can cause severe immunodeficiency and death to human beings. The spumaviruses cannot cause any disease to both human beings and animals since at the beginning of the formation of the retroviruses.
Viral Structure of Retroviruses
The viral structure of retroviruses contains an envelope that has particles of roughly 100mm as a diameter. The upper lipid envelop contains glycoprotein. The virions contain two identical single stands of RNA molecules. The two molecules stand as a dimer formed by base pairing between the two RNA molecules noted. All virions are similar, although retroviruses do not have the same morphology. Virion components include: Envelop: this envelope consists of the lipids obtained from the older plasma membrane in the budding process. The glycoproteins are also contained in the same envelope. This retroviral envelope plays the main three roles: the ability to enter directly into the cell by fusing with their membranes. RNA: The RNA genome has a terminal encoding section, which is vital in the replication. The RNA contains a dimer that has a cap on the fifth end. It is produced by the previous cell through polymerase II. The fifth end consists of 4 sections, namely, R, U5, PBS, and L. The U5 is a short series between R and PBS, while R is a short repeated sequence the useful in the reverse transcription that ensures the complete transition in the growing process.
On the other hand, PBS contains different bases the complement each other. The L is a region that gives an alert for the packaging of the genome RNA. Proteins: this consists of pol proteins and env proteins. Proctase is explained in different ways in different viruses. Retroviral gag proteins play a vital role in coordinating many aspects of assembling. The main function of protease in proteolytic cleavage during virion maturity to produce mature gag and pol proteins. Pol proteins are important in synthesizing viral DNA and integration into the parent DNA after the infections. Group antigen: proteins are the most components in the viral capsid (Hill et al., p 267). The most important role of the Gag proteins in the virion assembling is binding, reorganizing, and packaging the genome retroviral of the RNA.
The Gag proteins possess two different nucleic capsid binding domains, namely; matrix and nucleocapsid. Therefore the retrovirus must give out its changes in the phospholipids for it to use the enzyme of the infection in the cell to do its work because of the abnormal nature of forming the DNA. Since viruses are obligated to intracellular pathogens, they cannot multiply in the host cell’s metabolism absence. Though the replication life cycle of viruses disagrees totally in different species, several stages are essential for viral multiplication. They include; viral attachment: the viral proteins on the capsid envelope interact with certain receptors on the host cell’s layer. Mostly this determines the tropism of the viruses. Penetration: DNA viruses can also get inside of the host cell via receptor-mediated endocytosis. Therefore the process of attachment of the DNA viruses to a specific receptor can lead to a similar change in viral phospholipid proteins or the lipid envelop that can cause the fusion of the cell’s ral and cellular membrane oUp coating: the viral phospholipid is completely changed by a viral enzyme or host enzymes producing the viral genomic nucleic acid. Replication: since the viral genome has been uncoated, the translation of its viral genome is initiated. This is when the viral replication differs completely between the viruses of DNA and the RNA. The culmination process of the viral proteins and genome in the de novo synthesis is finally reached. Assembly: this is also called the maturation process. The viral proteins are packaged in the currently multiplied viral genome into newly formed virions that are easy to release from the host cell.
The virion release process involves two methods, namely; lysis and budding. Lysis leads to the death of the infected cells. The type of viruses involved is called cytolytic. Budding leads to the acquisition of the viral phospholipids envelop. The viruses from this process do not lead to the death of the infected cells, and therefore, they are known as cytopathic viruses. After the process of the virion release, some viral proteins remain in the host cell membrane. This acts as a potential of the targeted calculating antibodies. The cell that remains in the host cell’s cytoplasm can be processed and presented at the cell’s surface on class 1 molecules where they are recognized by the T cells of the host cell.
HIV is a virus that attacks the CD4 counts in the body. The CD4 counts are a white blood cell that fights against the infections attacking the body. These viruses can be transmitted through body fluids, and the condition is lifelong. The process may continue over a long period, but it slows down the progression once the treatment is initiated. HIV viruses weaken the immunity of the body. There are two types of HIV. They include HIV1 and HIV2. The two types of HIV are long-life, but effective treatment may make the victims have healthy lives. Understanding the difference between the two types of HIV helps increase the awareness of the progression. HIV 1 is the most common type of HIV, and many people are living with it. It occurs in most parts of the world. Both HIV1 and 2 are retroviral and have the same effects on the bodies of human beings. This means that not all treatments can work in both infections.
HIV Replication Cycle
HIV infection has different phases. Namely: Primary infection: this is a stage where the victim looks healthy, but the virus has already entered the body. So no one can notice it. Window stage: here, the patient tests negative for HIV, but the illness is asymptomatic. Seroconversion stage: in this stage, the HIV test is positive. The asymptomatic stage is the period between the onset of HIV/AIDs related illness and the seroconversion. Most people remain healthy. The CD4 count is above 500 cells/ml. AIDs related illness; this is the period between the onset of illness and diagnosis of AIDs. The CD4 count at this stage is between 500-200 cells/ml. AIDs: this is the final; stage of HIV, which is called frank AIDs. The CD4 count is below 200 cells/ml. The viral load is high, and the person infectious.
Pathogenesis/ Typical Time course of HIV Infection and Diagnosis
The diagnosis for HIV is the generic difference between HIV1 and HIV 2 whereby if a person takes a test for HIV 1, it may never detect HIV 2. Most people who are at risk are the ones with HIV 2. Both HIV 1 and HIV 2 lead to opportunistic diseases such as respiratory infections, for instance, pneumonia, skin infections, candidiasis, and gastro-intestinal like diarrhea. The HIV/ AIDs affects the immune system of a human being by attacking the CD4 cell, the antibodies produced by the immune system being unable to overcome the infections, weakening the immune system which cannot defend the body from opportunistic diseases, over time the HIV progressively weakens the immune system, the body becomes vulnerable of the varieties of the diseases such as cancer. Finally, the weak body is overwhelmed by the infections and dies (Hill et al., p.285). The high death rates associated with HIV/AIDs infections have triggered the health works to develop a mechanism of administering the antivirus drugs.
Mechanism of Antivirus Drugs and Antivirus Drug Resistance
Antiviral drugs are used for the treatment of viral infections. These drugs help HIV victims to live a longer life despite contracting the diseases. Some of the antivirus drugs (ARVs) objectives entail to prolong and improve the quality of life, suppress the virus, minimize the drug transitivity and side effects, and finally, in optimizing and extending the optimization of the usefulness of the other therapy.
Most antiviral drugs focus on a certain virus, while spectrum antiviral drugs are effective in a wide range of different viruses. Unlike in most antibiotics, antiviral drugs do not destroy their targeted pathogens, but they inhibit their development. Antimicrobials are classified as antiviral drugs, which also include antibiotics, antibacterial. Most of the antiviral drugs are perceived as relatively harmful to the human being’s body, and therefore, they can be used to treat the infections. Antiviral drugs should be differentiated from the viricides, which are not medication but deactivator or a destroyer of the virus particles either in or out of the human body. A diseased susceptibility can depict the body’s resistance to a certain antiviral drug to a drug brought about by a change in viral genotypes. The constant change of the genetic make-up can make a virus to be resistant to the available treatments. Viruses can resist the mechanisms throughout the antiviral treatment.
The development of the antiviral drug mechanism depends on the nature of the questionable virus. Some of the viruses, such as influenza, have a high error rate. Billions of the viruses are produced every day during infection. With each of the formed viruses replicating, then this is a possible cause of the resistance. In the event of the viruses’ recombination, like in influenza, the joining of two or more viruses plays a vital role in antiviral drugs’ resistance. The antiviral resistance is generally known to occur if mutations to the neuraminidase proteins hinder the NAI’s binding. The resistance of an antiviral drug is possible to all the viruses. Therefore, the mechanisms of the resistance of the antiviral drugs differ among the types of viruses. A national and international survey has been done to determine the effectiveness of the new FDA-approved antiviral drugs for the flus. The world health organization (WHO) has further given out the recommendations on the investigation regarding controlling the potential transmission of resistant viruses and preventing them from progressing in the future. Due to the ability to treat and detect the resistance of these antiviral drugs, an establishment of the strategies on how to combat the inevitability of the antiviral resistance emergence(Hill et al., p362).
The most convenient method of treating these resistant viruses is the combination of therapy, which uses different antivirals in one treatment. The treatment mechanisms, therefore, should give an account for the selection of resistant viruses. Viruses can also be screened if it is resistant to the drugs before the treatment is started. This helps minimize the frequencies of the exposures to unwanted antiviral, and it also ensures that the necessary medication is in use. These methods assist in improving the patient’s outcomes and detecting a new resistant mutation during the day-to-day activities of scanning. In conclusion, the virus can never replicate on its own, and therefore it requires a host cell’s DNA for the replication to occur (Gifford et al., p 334). In the replication process, cells such as granulocytes cells, macrophygen cells, T-helper cells, dendritic cells, and innate cells play a major role.
The replication of HIV viruses also requires a host cell. HIV may test positive or negative depending on the stage in which the patient is in. A negative test may not necessarily mean that a patient has not contracted the disease. The amount of the CD4 count in the body helps to know the stage of the HIV that a patient is in.
The mechanisms of administering the antiviral drugs to the patient differ according to the type of the viruses. The resistance of antiviral drugs is inevitable. There may be some cases of mutations in the body, and therefore this could be a possible reason for the resistance. Combined therapy is recommended for such situations to prevent such resistance of the viruses to the antiviruses.
Work Cited
Hill, Alison L., et al. “Insight into treatment of HIV infection from viral dynamics models.” Immunological reviews 285.1 (2018): 9-25.
Stephenson, Sarah E., et al. “Pericytes as Novel Targets for HIV/SIV Infection in the Lung.” American Journal of Physiology-Lung Cellular and Molecular Physiology (2020).
Gifford, Robert J., et al. “Nomenclature for endogenous retrovirus (ERV) loci.” Retrovirology 15.1 (2018): 1-11.
Trypsteen, Wim, et al. “Differential expression of lncRNAs during the HIV replication cycle: an underestimated layer in the HIV-host interplay.” Scientific Reports 6 (2016): 36111.
Rumlová, Michaela, et al. “Does BCA3 Play a Role in the HIV-1 Replication Cycle?.” Viruses 10.4 (2018): 212.