@Grace42Thorn @janieyaya @MartinaSisters ➡️1) Probable, not all retroviruses cause cancer, but all RNA tumor viruses are retroviruses.
They transform an infected cell by the action of one or more genes, which are present in the viral genome and are called viral oncogenes...
@Grace42Thorn @janieyaya @MartinaSisters 2) RNA viruses, known as retroviruses, which can induce the neoplastic transformation of eukaryotic cells. Examples are the Rous sarcoma virus, the feline leukemia virus, the avian erythroblastosis virus, etc ...
@Grace42Thorn @janieyaya @MartinaSisters 3) The RNA of the virus is made up of:
👉gag = gene that codes for a precursor protein which, once cut, produces the proteins of the viral particle.
👉pol = gene that codes for reverse transcriptase, an enzyme that has the task of transcribing single-stranded RNA to
@Grace42Thorn @janieyaya @MartinaSisters 4) double-stranded DNA.
👉env = gene encoding the glycoproteins of the viral envelope, called envelope.

➡️For example the Rous sarcoma virus, has an additional gene called 👉v-src (which has eukaryotic origins) and finds its counterpart in👉 c-src, a gene that
@Grace42Thorn @janieyaya @MartinaSisters 5) is very conserved throughout the animal kingdom. C-src is a gene that regulates cell proliferation in response to mitotic stimuli; this type of genes is called proto-oncogene.

➡️If this proto-oncogene were to undergo mutations, it would turn into oncogene, that is, a gene
@Grace42Thorn @janieyaya @MartinaSisters 6) responsible for the uncontrolled proliferation typical of a tumor cell.
Therefore 👉v-src is precisely a mutated variant of 👉c-src, therefore when it is inserted by the virus in a cell chromosome, it stimulates the proliferation pathway, transforming the healthy
@Grace42Thorn @janieyaya @MartinaSisters 7) cell into a cancer cell.
This is broadly the mechanism, but the other retroviruses have not found a way to fit 4 genes within their envelope, hence the presence of a viral oncogene v-onc (such as v-src or v- erbA for the avian influenza virus) results
@Grace42Thorn @janieyaya @MartinaSisters 8) in the loss of one of the three genes required to complete the life cycle.
This makes them defective transforming retroviruses, i.e. retroviruses unable to complete a cycle on their own.
However, they can complete it with the help of a helper virus,
@Grace42Thorn @janieyaya @MartinaSisters 9) which gives them gag, pol or env. Non-transforming retroviruses (those that have only gag, pol, and env in their RNA) also have the ability to turn a healthy cell into cancerous, but with a much lower probability than transforming viruses.
@Grace42Thorn @janieyaya @MartinaSisters 10) ➡️The mechanisms by which this is possible are 2 and are called 👉gene activation and 👉insertional mutagenesis.

➡️ Foreword: Transformation mechanism of a transforming retrovirus. 👉When a virus infects a cell, its RNA genome is released from the viral particle along with
@Grace42Thorn @janieyaya @MartinaSisters 11) the reverse transcriptase. In the cellular cytosol, the enzyme synthesizes a complementary DNA strand (c-DNA), consuming the host's nucleotides.

This viral DNA is first translocated into the nucleus and then integrates into a chromosome in the following way. The 3 'and 5'
@Grace42Thorn @janieyaya @MartinaSisters 12) ends of the molecule contain repeated terminal sequences (LTRs), which contain numerous integration regulation signals.

Consequently, the insertion into the cell chromosome occurs as a result of the interaction of these LTRs with proteins that cut the cellular DNA.
@Grace42Thorn @janieyaya @MartinaSisters 13) LTR must generate messenger RNA for the synthesis, again at the host's expense, of the proteins encoded by gag, pol, env, and v-src.

➡️ Gene activation:

As they increase transcription of neighboring genes, LTRs also stimulate that of cellular genes
@Grace42Thorn @janieyaya @MartinaSisters 14)downstream of their location. So if we find c-src,this will be transcribed and translated in a constitutive way.
C-src encodes the protein kinase encoded by v-src,but endowed with its regulatory domain.
This is localized in the membrane and its presence stimulates mitosis.
@Grace42Thorn @janieyaya @MartinaSisters 15) ➡️ Insertional Mutagenesis:

This neoplastic transformation mechanism by a non-transforming virus involves the insertion of the genetic material within a cellular gene. This causes the gene affected by the insertion to lose function and consequently can
@Grace42Thorn @janieyaya @MartinaSisters 16) cause the cell to transform if the gene was a tumor suppressor or a mutator gene.

➡️ But there is also a👉 third mechanism produced synthetically in the laboratory.

SARS COV 2 has an unusual sequence 👉 "CCTCGGCGGGCACGT" which generates the "unknown region",
@Grace42Thorn @janieyaya @MartinaSisters 17) of artificial origin, between S1 / S2,👉 PRRAR motif "related to 👉modified polynucleotides for the production of 👉oncology-related 👉proteins and 👉peptides and methods 👉for improving immune control block therapy,👉 for modulation of the microbiome.
@Grace42Thorn @janieyaya @MartinaSisters 18) ➡️ PRRAR / S = is a cellular reprogramming code that SARS COV 2 RNA sends to cells and bacteria, for their subjugation, in a new mutant form.

👉The protein sequence 682-687 (PRRARS), in the S-type protein, is responsible for its correct binding with the
@Grace42Thorn @janieyaya @MartinaSisters 19) host proteases of 👉furin, 👉catepsin and 👉plasmin and the mutation of these residues compromises their interaction.

➡️ Biologists and biochemists already know that cleavage at the level of arginine residues is commonly used to activate a range of human proteins.


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More from @BidoliNicola

4 Apr
➡️ Cell reprogramming expressed through RNA-induced mutagenicity of #SARSCoV2 in infected cells confirmed.👇

1) SARS-CoV-2 is an enveloped beta-Coronavirus RNA belonging to the Coronaviridae family.

The genome is packaged inside a helical capsid formed by the
2) nucleocapsid (N) protein.

Three other structural proteins are associated with the viral envelope: membrane (M), envelope (E) and glycoprotein peak (S).

Cellular entry of SARS-CoV-2 depends on the binding of protein S to the angiotensin converting enzyme 2 (ACE2) which is a
3) specific cell receptor located on the surface of the host cell.

This receptor facilitates zoonotic transfer because these viruses can involve ACE2 from different animal species.

Beta-coronaviruses replicate in the cytoplasm; cellular compartments such as the
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➡️➡️➡️ Confirmed high level of identity of the FIPV, and with the SARS COV 2.👇

➡️1) FeCV-FIPV / HCoV-229E ratio; the non-random and non-natural interaction between these two coronaviruses has allowed the development of the SARS CoV 2 Chimera.
➡️ 2) The percentage of identity between FeCV-FIPV, and SARS CoV 2, is 👉44.0-44.5%, but if you use👉 NSP16 as a mediator, things change and you get to an identity percentage of 👉99.6-99 , 9%, between FeCV nsp16, and SARS CoV 2 nsp16.
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➡️D614G (Asp 614→Gly) as a replacement in S1, increased the ACE2 affinity, leading to 👉more infectivity and transmissibility.

➡️ There are non-synonymous nucleotide modifications, including 👉E484K, 👉N501Y and / or 👉K417N (Lys 417 → Asn) in the ACE2 interface of the RBD.
➡️ There are also various deletions in the amino (N) -terminal (NTD) domain of S1 in 👉B.1.1.7 and 👉B.1.351.

➡️ Although most mutations in these variants were observed in a smaller fraction of the SARS-CoV-2 sequences during the first year of the pandemic,
including 👉K417N, 👉E484K and 👉N501Y, there is no evidence to suggest that these variants have been created by adding sequences of each substitution during transmission between hosts.

➡️ As only a few SARS-CoV-2 mutations were in circulation during most of 2020, it is likely
Read 5 tweets
25 Mar
➡️1) (INSACOG) The Virologist 👉Shahid Jameel explained that a double mutation 👉in key areas of the virus's spike protein can increase these risks and allow the virus to escape the immune system; making the virus 👉more contagious and in some cases.
2) Is more probable that what emerged from my research 👉SARS COV 2 ORF 8 created a double mutation in the initial lineage.
👉The ORF8 protein has the characteristic of potentiating the virus and thus making it more virulent and infectious.
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23 Mar
@gerdosi @gadboit @SunshineLife_21 @FatEmperor ➡️ 1) The relationship of the "bacteriophage nature" in SARS COV 2 is the following. Let's start from the meaning of a bacteriophage; they are obligate intracellular parasites, that is, they can ONLY survive using the resources of a host cell.
@gerdosi @gadboit @SunshineLife_21 @FatEmperor 2) They are capable of infecting all types of cells including 👉bacteria. When at the end of February 2019 I saw the photos of SARS COV 2, taken by the Marx Plank Institute, I was amazed. In this photo you could see how a tissue, affected by SARS COV 2, changed its shape creating
@gerdosi @gadboit @SunshineLife_21 @FatEmperor 3) sprawling filaments that responded to I don't know what genetic code of the virus. This photo always remained in my head until, after endless reading of papers dedicated to the topic in question, I came across this
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23 Mar
1) ➡️ The application detected four highly specific signature sequence regions that hit all 25 (available at the time of analysis) 👉Wuhan genomes.
➡️The detected signatures were found to occur in disparate locations on the genome. 👇 Image
2) ➡️ All four signatures were found to target all current 👉Wuhan genomes, and three out of four of these signature regions did 👉NOT sufficiently align to any known coronavirus or other organism in 👉NCBI BLAST databases.👇 Image
Read 15 tweets

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