Viruses are mostly recognized by toll like receptor (TLR-3), activate various pathways such as NFKB, MAPK etc which leads to transcription and produce Interferon's. So, IFN alpha is the first response.

Hi,

The answer is Interferon alpha which activate by some various pathways.

IFN-alpha production is the first immune response to any virus infection....it is non specific and most cells can produce IFN-alpha upon viral infection...NK cells will take some time for their action...

Of course IFN-alpha is the first line of defense against virus and as it has been mentioned it can be activate by various pathways. However the answer also depends by what do you mean by immune response? If you mean specific immune response then the answer mainly depends of the virus type. For some the specific immune response is mainly drivent by humoral immunity or for other is cell-mediated immune response.

Role of Interferon alpha comes earlier than NK cells. Interferon alpha helps to activate immune cells like NK cells and macrophages against infections.

IFN-alpha is secreted from virally infected cells via several signal pathways as a first line immune defense against virus infections. NK cells are part of innate immunity and need to be activated by cytokine IL-12 -which is secreted from activated macrophages- to get rid of virally infected cells.

 Interferon alpha comes earlier than NK cells. It helps to activate NK cells.

By and large I agree with the above responses to the question above (as it is worded). I would like to add that we need to consider additional factors in describing activation of an immune response following a viral infection. The factors such as type of virus, target cell for the virus in question, and the type of innate immune response. In general, most cells can produce constitutive detectable levels of IFN-alpha (also referred as leukocyte IFN). However, the majority of IFN-alpha (up to 1,000-fold more) is produced by innate immune cells (for example, dendritic cells). If virus has the ability to infect fibroblasts (mesenchymal cells), these cells mainly produce the IFN-beta (also referred as fibroblast IFN) upon infections with DNA and RNA viruses. Because IFN-alpha and IFN-beta regulate each others expression in a variety of cell types, it may be appropriate to indicate that both types of IFNs are induced by virus infected cells.

First.  IFN alfa which is due to innate=inborn nonspecific immunity..then..IgM antibodies which switch over in ti IgG...later on..

IgG,IgM ,IgE,Interferons and lymphocytes etc...

IFNa

Hi Mohammad, 

NK cells are not in steady state (they are at barely detectable levels) in peripheral tissues like muscle, skin, etc. NK cells are not the initial source if the infection/vaccination is there. Cells like fibroblasts and most of non immune cells express sensors for viral infection, like PKR, cGAS, STING, etc, that when they get activated block translation and induce type I interferons. If you want to get into more detail read 

http://www.sciencedirect.com/science/article/pii/S0952791514001496

The initial immune response, I don't believe is identical for all viruses. For example, RNA viruses that require reverse transcription into the host cell's DNA before replication would elicit different response cascade from large protein capsid DNA viruses. In some cases cellular mediated immunity may be activated before a strong humoral (Ig)  response. I have my own theories on antigen processing but without getting into that, it is safe to say that the cascade of immune responses is not necessarily uniform for all viruses.

Surely IFNa

I believe NK cells are much slower than IFN alpha , requiring much more time for activation and killing responses.

IFN alpha secretion for sure is more intense and faster

Complement components are also implicated in defense against viral antigens. 

interferon alpha@

The immune response that develops in a viral infection is first given by the innate immune response. The virus enters the cell and deposits its genetic material that is recognized by endosomal TLRs (TLR3, 7, 8, 9) or by proteins of intracytoplasmic recognition (MDA-5, RIG-1 and DAI) of foreign DNA and RNA, these proteins recognizing foreign nucleic acid will activate the kinase proteins that will then activate the transcription of IRF (interferon regulation factor, IRF1,3 and 7 ) that enters the cell nucleus and activates the transcription of interferon type I (alpha and beta). This cell will produce type I interferon that comes into contact with neighboring uninfected cells by interferon I and II receptors, getting the cell into an antiviral state. This state is caused by the activation of the transmission pathways of jack-stat signals that induce the expression of genes whose products interfere with the replication of the virus in uninfected cells. We must remember that type I interferon (alpha and beta) increases MCH-I expression, activates NK cells and promotes differentiation of Th virgin lymphocytes to Th1.

I hope the information provided helps you, regards.

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La respuesta inmune que se desarrolla en una infección viral se da primeramente por la respuesta inmune innata. El virus ingresa a la célula y deposita su material genético que es reconocido por los TLR endosomicos (TLR3, 7, 8, 9) o por las proteínas de reconocimiento intracitoplasmatico (MDA-5, RIG-1 y DAI) de ADN y ARN extraño, estas proteínas al reconocer ácido nucleico extraño activaran las proteínas cinasas que luego activaran la transcripción de IRF (factor de regulación del interferón, IRF1,3 y 7) que ingresara al núcleo celular y activara la transcripción de interferón de tipo I (alfa y beta). Esta célula producirá interferón de tipo I que entrará en contacto con las células vecinas no infectadas mediante los receptores de interferón I y II, consiguiendo que la célula entre en un estado antivírico. Este estado se da por la activación de las vías de transmisión de señales jack-stat que inducen la expresión de genes cuyos productos interfieren en la replicación del virus en las células no infectadas. Debemos recordar que el interferón de tipo I (alfa y beta) incrementa la expresión de MCH-I, activan las células NK y promueven la diferenciación de los linfocitos Th vírgenes a Th1.