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Influenza viruses of A, B and C types are responsible for globally spreaded human infections. These consist of Ribonucleic acid segments (RNA-segments), heterotrimeric RNA-polymerase and nucleoprotein counterparts (altogether, Ribonucleo peptides or RNPs). Subtype of A and B infections increases severity of diseases and interact with CD8+ T-cells to generate immunogenic responses. Exact cross-reactivity features of influenza subtypes are not similar; although, entry of influenza virus in host cells and replication process of the virus are similar. This presentation aims to reflect cellular processes of influenza infections in humans, which affects their quality of life, health and wellbeing. It also demonstrates what Australia is thinking today to combat influenza pandemic, which snatches thousands of lives in every year.


This presentation considered information from two scholarly journal articles within last five years to illustrate the scenario on human wellbeing.

Influenza interaction with human cells

Influenza viruses target growth factor receptors (GFR) of human cells for initiating
viral infection processes. Fibroblast Growth Factor Receptors or FGFRs act as cofactors for
triggering cellular invasion of Influenza viruses (Dou et al. 2018). Binding of virus with
GFR’s extracellular domain (hemagglutinin-domain) aids in internalization processes with
formation of endosomes (viral coated).
● In one way, GFR activation signals for suppressing genes of interferon-mediated
immune response mechanisms.
● On the other hand, coated endosomes fuse with lysosomes for vesicle acidification
and fusion within cytosol (Dou et al. 2018).
Thus, viral genome fragments and RNPs trigger Nuclear Localization Signals or NLS
via conjugation of importin-α (adapter) for entering into nucleus.
Within nucleus, viral RNA-pol activities are noted for continuing replication and
transcription machinery. Here, complementary RNA strands are built first, followed by viral
RNAs with those templates.
After assembly of genes, further cycles of genomic replication occur and:
● Newly synthesized RNPs exit nucleus with help of Rab11-associated vesicle transport
towards endoplasmic reticulum (ER) (Dou et al. 2018).
● Within ER, viral non-genomic proteins are synthesized and assembled for developing
viral replicas.
● Finally, these replicas exit cells with help of hemagglutinin residues of membrane
(Dou et al. 2018).
Constant invasion of viruses within human cells, replication of viral replicas within
those cells and release of viruses in bloodstream increases viral loads in blood.

Clinical symptoms

● Fever
● Sore throat
● Headache
● Fatigue
● Muscle pain
● Dizziness, nausea
● Diarrhea and vomiting (sometimes)

Cellular targets for influenza infection treatments

Monoclonal antibodies or mAbs:

Monoclonal antibodies targeted to GFR receptors would be able to prevent viral entry
in host cells. These antibodies block ligand-binding domains of GFRs inside cells, which
block receptor dimer formation and entry of viruses via hemagglutinin residue interactions
(Hondermarck et al. 2020).

Examples: Cetuximab and Trastuzumab

Tyrosine Kinase receptor blockers:

GFRs trigger cell signaling by Tyrosine Kinase activity. These blockers act in a competitive inhibition mechanism inside cell, which prevent ATPs from binding with ATPbinding pockets of Tyrosine Kinases. As a result, GFR receptor activation and dimerization are not possible, which prevents viral entry inside cells (Hondermarck et al. 2020).GFRs trigger cell signaling by Tyrosine Kinase activity. These blockers act in a competitive inhibition mechanism inside cell, which prevent ATPs from binding with ATPbinding pockets of Tyrosine Kinases. As a result, GFR receptor activation and dimerization are not possible, which prevents viral entry inside cells (Hondermarck et al. 2020).

What is Australia thinking now?

Seasonal flu in summer or Influenza creates an epidemic for Australia, every year.
These can be triggered by avian strains, as well as human specific strains. Thus, developing
potential targets for preventing flu-oriented diseases are prime targets for Australian research

Since Sars-Cov-2 virus’s structure is almost similar to Influenza virus, Australia is
trying to test pharmacological targets of influenza in covid cases to examine efficiency
(Hondermarck et al. 2020). Notably, it is driving promising trials by involving GFR-targets
of cells to prevent entry of Sars-Cov-2 virus inside host cells. Further, drugs targeted to
coreceptor FGFRs are also in notion. Thus, following candidates are promising agents for
future influenza and Covid-19 related research:


Influenza virus hijacks cellular machinery of humans for their own survival and
replication, which in turn enhances viral load in blood. Therefore, pathogenicity occurs that
could be reflected by affecting human health and wellbeing. Recent outbreak of Covid-19
virus shifted treatment focus on influenza, which is an existing threat to humans. Further, due
to symptom similarities, many people are panicked with Covid infections while they are
suffering from influenza infections. However, immediate attention regarding treatment is
necessary in both cases.

Maddox Smith

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