How HCMV Evades the Human Immune Response

How HCMV Evades the Human Immune Response

Herpes virusna infekcija pasa je teška, često fatalna infekcija štenaca u prvim nedeljama života, dok je kod pasa starijih od 3 nedelje infekcija retka ili je bez kliničkih simptoma. W stawach najczęściej występuje u karpi dwuletnich (rzadziej u kroczka). RNA viruses have RNA (ribonucleic acid) as their genetic material and are usually single stranded, whereas, DNA Viruses have DNA (deoxyribo nucleic acid) as their nucleic acid and are usually double stranded. 240 5 11 bear here. Anyone who has had chickenpox can develop shingles because VZV remains in the nerve cells of the body after the chickenpox infection clears and VZV can reappear years later causing shingles. This virus can be potentially life-threatening in immunocompromised people, “such as HIV-infected persons, organ transplant recipients, or newborn infants” [1]. x, 1327 pp.

This virus is spread through the transfer of bodily fluids: urine, saliva, blood, tears, semen, and breast milk [1]. The evasion of the host immune response has recently been the topic of discussion in Rocky Mountain College’s Virology course. Crea ca. A further two viruses found in the night monkey are tentatively placed in the Cytomegalovirus genus, and are called Herpesvirus aotus 1 and Herpesvirus aotus 3. HCMV has many different proteins. (We can only see the smallest part of the large) Infinite repetition of power distribution and allocation with an absolute assuredness of uniqueness and identity. So infected cells are not able to express the receptors needed to grab the attention of NK cells and activate them, plus, the protein that puts out a warning to NK cells to come help is degraded so it does not work either.

How HCMV Evades the Human Immune Response
Two cells (centre-left) have the characteristic (cytoplasmic) viral inclusion bodies (small pink globules). HCMV proteins are also capable of subduing apoptosis of cells. Apoptosis is programed cell death and is detrimental for a virus because it limits the spread of the virus. HCMV proteins UL36 and UL37 “prevent apoptosis of infected cells, promoting its dissemination within the host” [3]. Figure 2 summarizes some of the ways HCMV evades the human immune response, including what was just discussed. Herpesviruses. also discusses how pTRS1 and pIRS1 in HCMV cause the nuclear accumulation of PKR during viral infection these proteins cause PKR to remain inactivated [5].

The main migration is in May, when around 1.5 million animals move from the plains to the woods; they return in November as summer rains water the plains. So in other words, PKR moves from the cytoplasm into the nucleus because of HCMV proteins and therefore PKR is inhibited. Duck herpesvirus 1 causes duck plague. Overall, HCMV has many mechanisms to help it evade the host immune response. In order to find out all this eye-opening data, multiple tests had to be done in controlled environments. One of those tests included indirect immunofluorescence [5]. Immunofluorescence (IF) tests are an assessment of cells in order to look for specific proteins;   they do this by conjugating florescent dyes onto antibodies, and then the antigen you are looking for can be found using fluorescence techniques [6].

Proteins were also separated using SDS-PAGE, which is just a polyacrylamide gel electrophoresis (PAGE) with sodium dodecyl sulfate (SDS) to linearize proteins and to give a negative charge. Data was then quantified using a flow cytometer. This machine uses lasers to count the amount of cells and to sort out the different types of cells [7]. (5a) Virussen zijn niet-cellulair. This is a specialized type of flow cytometry where in addition to having the “ability to label and identify individual cells via fluorescent antibodies, cellular products such as cytokines, proteins, and other factors may also be measured as well” [7]. These tests and machines allow for the best research possible to study HCMV. Overall there is much information regarding how many ways HCMV can evade the host immune response.

The more detailed molecular information we know about the HCMV, the more likely we can come up with a way to combat this virus. One of the focuses on future experiments should be finding a way to decrease the chances of people dying from getting this virus while they are immunocompromised. sapiens is the only surviving species of the genus Homo. Also, one discovery that has yet to be made could be to make a clinical treatment to help find a way to inhibit some of this virus’s leading proteins that cause our immune system to falter if we are immunocompromised.

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