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Influenza virus and cell signaling pathways.

Gaur P, Munjhal A, Lal SK - Med. Sci. Monit. (2011)

Bottom Line: Influenza A virus, due to its segmented RNA genome, is highly subject to mutation, resulting in rapid formation of variants.Infected cell pathways are hijacked by an array of intracellular signaling cascades such as NF-κB signaling, PI3K/Akt pathway, MAPK pathway, PKC/PKR signaling and TLR/RIG-I signaling cascades.This review presents a research update on the subject and discusses the impact of influenza viral infection on these cell signaling pathways.

View Article: PubMed Central - PubMed

Affiliation: Virology Group, International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Road, New Delhi, India.

ABSTRACT
Influenza viruses comprise a major class of human respiratory pathogens, responsible for causing morbidity and mortality worldwide. Influenza A virus, due to its segmented RNA genome, is highly subject to mutation, resulting in rapid formation of variants. During influenza infection, viral proteins interact with host proteins and exploit a variety of cellular pathways for their own benefit. Influenza virus inhibits the synthesis of these cellular proteins and facilitates expression of its own proteins for viral transcription and replication. Infected cell pathways are hijacked by an array of intracellular signaling cascades such as NF-κB signaling, PI3K/Akt pathway, MAPK pathway, PKC/PKR signaling and TLR/RIG-I signaling cascades. This review presents a research update on the subject and discusses the impact of influenza viral infection on these cell signaling pathways.

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Related in: MedlinePlus

Host cell machinery gets activated during influenza infection and leads to trigger Signaling pathways. Influenza is know to produce early and late viral proteins post infections. NS1, NP, PB1, PB2 are early protein and synthesize in 0–5 h.p.i. HA, NA, M1, NEP, M2, PB1-F2 are late proteins and synthesize in 5–10 h.p.i. This process leads to the virus production in between 5–12 h.p.i. and followed apoptosis of the cells in 20 h.p.i. During this whole processes some of the pathways are know to induce: 1, PI3-Akt pathway; 2, NFkB/lkB pathway; 3, MAPK pathway (A, JNK pathway; B, p38 pathway; C, ERK1/2 patyhway; D, ERK5 pathway); 4, protein kinase C (PKC)/PKR signaling; 5, TLR/RIG-I signaling.Symbols used in the Figure: ⊣ inhibition; ⇢ unknown mechanism; → direct activation; ⇆ reversible process.
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f1-medscimonit-17-6-ra148: Host cell machinery gets activated during influenza infection and leads to trigger Signaling pathways. Influenza is know to produce early and late viral proteins post infections. NS1, NP, PB1, PB2 are early protein and synthesize in 0–5 h.p.i. HA, NA, M1, NEP, M2, PB1-F2 are late proteins and synthesize in 5–10 h.p.i. This process leads to the virus production in between 5–12 h.p.i. and followed apoptosis of the cells in 20 h.p.i. During this whole processes some of the pathways are know to induce: 1, PI3-Akt pathway; 2, NFkB/lkB pathway; 3, MAPK pathway (A, JNK pathway; B, p38 pathway; C, ERK1/2 patyhway; D, ERK5 pathway); 4, protein kinase C (PKC)/PKR signaling; 5, TLR/RIG-I signaling.Symbols used in the Figure: ⊣ inhibition; ⇢ unknown mechanism; → direct activation; ⇆ reversible process.

Mentions: The NFκB/IκB pathway plays a vital role in mediating inflammation, immune response, proliferation and apoptosis [14,15]. NF-κB is a nuclear factor κB, a transcriptional factor which plays a central role in promoting the expression of more than 150 genes, which in turn governs the cellular status of genes encoding cytokine/chemokines, adhesion molecules and anti/pro-apoptotic genes [6,16]. NF-κB is present as a complex with its inhibitor IκB. For release from this complex, activation of IKK is required [17]. The IKK complex is composed of active IKK1/IKKα, IKK2/IKKβ and scaffold protein NEMO (NF-κB essential modulator)/IKKγ [15]. Upon activation, IKK phosphorylates and degrades the IκB protein [18], which leads to the release of transcriptionally active NF-κB subunits p65/p50 from the inhibitory complex which translocate into the nucleus, where they can ‘turn on’ the expression of specific genes that have DNA-binding sites for NF-κB in their promoters [18,19] (Figure 1(2)). IKK2 degrades the IκB and activates NF-κB, while IKK1 primarily phosphorylates the other factors of the NF-κB family, such as p100/p52 [15].


Influenza virus and cell signaling pathways.

Gaur P, Munjhal A, Lal SK - Med. Sci. Monit. (2011)

Host cell machinery gets activated during influenza infection and leads to trigger Signaling pathways. Influenza is know to produce early and late viral proteins post infections. NS1, NP, PB1, PB2 are early protein and synthesize in 0–5 h.p.i. HA, NA, M1, NEP, M2, PB1-F2 are late proteins and synthesize in 5–10 h.p.i. This process leads to the virus production in between 5–12 h.p.i. and followed apoptosis of the cells in 20 h.p.i. During this whole processes some of the pathways are know to induce: 1, PI3-Akt pathway; 2, NFkB/lkB pathway; 3, MAPK pathway (A, JNK pathway; B, p38 pathway; C, ERK1/2 patyhway; D, ERK5 pathway); 4, protein kinase C (PKC)/PKR signaling; 5, TLR/RIG-I signaling.Symbols used in the Figure: ⊣ inhibition; ⇢ unknown mechanism; → direct activation; ⇆ reversible process.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3539548&req=5

f1-medscimonit-17-6-ra148: Host cell machinery gets activated during influenza infection and leads to trigger Signaling pathways. Influenza is know to produce early and late viral proteins post infections. NS1, NP, PB1, PB2 are early protein and synthesize in 0–5 h.p.i. HA, NA, M1, NEP, M2, PB1-F2 are late proteins and synthesize in 5–10 h.p.i. This process leads to the virus production in between 5–12 h.p.i. and followed apoptosis of the cells in 20 h.p.i. During this whole processes some of the pathways are know to induce: 1, PI3-Akt pathway; 2, NFkB/lkB pathway; 3, MAPK pathway (A, JNK pathway; B, p38 pathway; C, ERK1/2 patyhway; D, ERK5 pathway); 4, protein kinase C (PKC)/PKR signaling; 5, TLR/RIG-I signaling.Symbols used in the Figure: ⊣ inhibition; ⇢ unknown mechanism; → direct activation; ⇆ reversible process.
Mentions: The NFκB/IκB pathway plays a vital role in mediating inflammation, immune response, proliferation and apoptosis [14,15]. NF-κB is a nuclear factor κB, a transcriptional factor which plays a central role in promoting the expression of more than 150 genes, which in turn governs the cellular status of genes encoding cytokine/chemokines, adhesion molecules and anti/pro-apoptotic genes [6,16]. NF-κB is present as a complex with its inhibitor IκB. For release from this complex, activation of IKK is required [17]. The IKK complex is composed of active IKK1/IKKα, IKK2/IKKβ and scaffold protein NEMO (NF-κB essential modulator)/IKKγ [15]. Upon activation, IKK phosphorylates and degrades the IκB protein [18], which leads to the release of transcriptionally active NF-κB subunits p65/p50 from the inhibitory complex which translocate into the nucleus, where they can ‘turn on’ the expression of specific genes that have DNA-binding sites for NF-κB in their promoters [18,19] (Figure 1(2)). IKK2 degrades the IκB and activates NF-κB, while IKK1 primarily phosphorylates the other factors of the NF-κB family, such as p100/p52 [15].

Bottom Line: Influenza A virus, due to its segmented RNA genome, is highly subject to mutation, resulting in rapid formation of variants.Infected cell pathways are hijacked by an array of intracellular signaling cascades such as NF-κB signaling, PI3K/Akt pathway, MAPK pathway, PKC/PKR signaling and TLR/RIG-I signaling cascades.This review presents a research update on the subject and discusses the impact of influenza viral infection on these cell signaling pathways.

View Article: PubMed Central - PubMed

Affiliation: Virology Group, International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Road, New Delhi, India.

ABSTRACT
Influenza viruses comprise a major class of human respiratory pathogens, responsible for causing morbidity and mortality worldwide. Influenza A virus, due to its segmented RNA genome, is highly subject to mutation, resulting in rapid formation of variants. During influenza infection, viral proteins interact with host proteins and exploit a variety of cellular pathways for their own benefit. Influenza virus inhibits the synthesis of these cellular proteins and facilitates expression of its own proteins for viral transcription and replication. Infected cell pathways are hijacked by an array of intracellular signaling cascades such as NF-κB signaling, PI3K/Akt pathway, MAPK pathway, PKC/PKR signaling and TLR/RIG-I signaling cascades. This review presents a research update on the subject and discusses the impact of influenza viral infection on these cell signaling pathways.

Show MeSH
Related in: MedlinePlus