Because this virus H7N9 can really be a future trouble, I tried to find out something or anything from WHO sources which could highlight the situation of to day and I found this:


Analysis of recent scientific information on avian influenza A(H7N9) virus
10 February 2017
Monthly Risk Assessment Summary – Influenza at the Human-Animal Interface”

1Influenza at the human-animal interface (HAI)    Summary and assessment,

22 Januaryto 12 February2019

•New infections 1:

Since the previous update on 21 January 2019, two human infections with avian influenza A(H9N2)viruses and one human infection with an influenza A(H3N2) variant virus were reported.

•Risk assessment:

The overall public health risk from currently known influenza viruses at the human-animal interface (HAI) has not changed, and the likelihood of sustained human-to-human transmission of these viruses remains low.

Further human infections with viruses of animal origin are expected.

•Risk management:

Selection of new candidate vaccine viruses (CVVs) for zoonotic influenza for influenza pandemic preparedness purposes was done during a recent WHO consultation.2

•IHR compliance: All human infections caused by a new influenza subtype are required to be reported under the International Health Regulations (IHR, 2005).3

This includes any influenza A virus that has demonstrated the capacity to infect a human and its heamagglutinin gene (or protein) is not a mutated form of those, i.e. A(H1)or A(H3), circulating widely in the human population. Information from these notifications is critical to inform risk assessments for influenza at the human-animal interface.

Avian Influenza Viruses

Current situation:

Avian influenza A(H5) viruses

Since the last update on 21January 2019, no new laboratory-confirmed human cases of influenza A(H5) virus infections were reported to WHO. According to reports received by the World Organisation for Animal Health (OIE), various influenza A(H5) subtypes continue to be detected in birds in Africa, Europe and Asia.Overall, the risk assessment has not changed.

Avian influenza A(H7N9) viruses

Since the last update on 21 January2019, no new laboratory-confirmed human cases of influenza A(H7N9) virus infections were reported to WHO. There have been no publicly available reports from animal health authorities in China of influenza A(H7N9) virus detections in animals in recent months.4,5

Overall, the risk assessment has not changed

The News I read at late night was pictured by a photo from China with the sign “A H7N9” and “Swedish doctors are considering that virus A H7N9 as mysterious” . It has been only in some birds sometimes even here in Sweden. So until now – 28th March 2019 I dont find any rapport of any human cases of novel flu in Sweden, yet. in this double novel antigen reassortment form. In Eastern Finland there is now much influenza and 6 people has been killed by virus, but the name of virus was not in the News to day. So any how because of Chinese lethalities there is an alert for this virus A H7N9 all over the world.

It seems so that this  novel Avian influenza A (H7N9)   is not contended with  conventional  compartments of Human body but  has multiorgan  targeting character.   This is my  personal opiinion.    New  strategies perhaps are to be developed  in the therapy and-  prophylax.   E.g.  it may be  good to keep  infected ones at home so  a long time as possible and to have a good  reserves at home ( food items,  some medicines). Alsp the healthy ones should not   go to do shopping   very freequently. every day in big  multitudes of people, if they  make real reserves for  food  for  their home  —  Until now, this was  the first time , yesterday 27th  March , that I saw  in one newspaper,  News about that   there are som cases of  human A H7N9 in Sweden. It seems ,  an  ARDS- case,  at least  in one person  of them. And this  virus is called “mysterious” and characterized as A H7N9.

Citate :
Horst Ibelgaufts. Dictionary of Cytokines. 1995 VCH. Winham, New York, Basel, Cambridge, Tokyo. Page 434,

ITEM: IP-10 , immune protein 10
also gamma-IP10.
The expression of IP-10 from a variety of cells, including monocytes, endothelial cells, keratinocytes, and fibroblasts, is induced by IFNgamma and TNFalfa. The induction of the synthesis of IP-10 is used as an assay of IFNgamma activities.
The protein has a length of 98 amino acids. It shows homology to PF4 (platelet derived factor 4) and belongs to the chemokine family of cytokines.

IP-10 is also related to a gene called CRG-2 (CRG, cytokine responsive gene), which encodes a product that also belongs to the chemokine family of proteins.
The human IP-10 genes contains four exons and maps to chromosome 4q12-21 in the vicinity of the cytokine genes belonging to the chemokine family of proteins.

Gamma- IP10 has been detected in keratinocytes, lymphocytes, monocytes, and endothelial cells in immunologically mediated processes, such as positive tuberculin skin tests, and in growth-activated keratinocytes, such as in psoriasis.
Keratinocytes in normal epidermis do not produce gamma-IP10.
In vivo(mouse) IP-10 is synthesized predominantly in the liver and the kidney after intravenous injection of inflammatory agents, and in particular after injection of IFNgamma, and may play an important role in the response of liver and kidney to systemic inflammation.
IP-10 mRNA expression is more sensitive to suppression by IL4 when stimulated by bacterial lipopolysaccharides than by IFNgamma/IL2.

It has been suggested that IP-10 may play an important role in hypersensitivity reactions of the delayed type. Increased levels of IP-10 are found in psoriatic plaques characterized by infiltration of neutrophils, IP-10, however, does not activate neutrophils.

IP-10 probably also plays a role in regulation of the growth of early hematopoetic progenitor cells. It has been shown to suppress in vitro colony formation of highly enriched CD34-positive cells in the presence of SCF, GM-SCF or SCF+ EPO, but not in their absence with the expection of SCF.

Tumor cells genetically engineered to express high levels of murine IP-10 have been shown to elicit a powerful host-mediated antitumor effect in vivo which appears to be mediated by the recruitment of inflammatory infiltrates composed of lymphocytes, neutrophils, and monocytes.

Muistiin 28.3. 2019


Citate :

Horst Ibelgaufts. Dictionary of Cytokines. 1995 VCH. Winham, New York, Basel, Cambridge, Tokyo. Page 503.


  • MCP = Monocyte chemotactic protein. This factor is encoded by the human JE gene.

It is chemotactic for monocytes ( See: Chemotaxis).

This factor is identical with

MCAF ( monocyte chemotactic and activating factor),

MCP-1 ( monocyte chemotactic protein 1),


SMC-CH ( smooth muscle cell chemotactic factor),

LDCF ( lymphocyte derived chemotactic factor),

GDCF ( glioma-derived monocyte chemotactic factor),

TDCF ( tumor-derived chemotactic factor).

MCP belongs to the chemokine family of cytokines. It has been shown to bind to a receptor called CKR-1 ( chemokine receptor 1).

  • (MCP-1 – MCP-2; microbicidal cationic protein.

These microbicidal proteins have been isolated from rabbit lung macrophages. They are identical with the defensins NP-1 and NP-2, respectively).

  • MCP-1; monocyte chemoattractant protein-1.

MCP-1 is encoded by the human JE gene at chromosome 17q11.2-q21.2, also known as SCY A2 ( small inducible cytokine A2). Antibodies directed against murine MCP-1 cross-react with the human factor. The human factor is 49 amino acids shorter at the aminoterminus than the rodent factor.

MCP-1 belongs to the chemokine family of cytokines.

(Many names!)

It is identical with MCAF (monocyte chemotactic and activating factor).

MCP-1 ( monocyte chemotactic protein 1),


SMC-CH (smooth muscle cell chemotactic factor),

LDCF (lymphocyte derived chemotactic factor),

GDCF (glioma-derived monocyte chemotactic factor),

TDCF ( tumor-derived chemotactic factor),


MCP-1 shows a high degree of homology with MARC protein.

MCP-1 is expressed by monocytes, vascular endothelial cells, smooth muscle cells, glomerular mesangial cells, osteoblastic cells, and human pulmonary type II-like epithelial cells in culture.

It is constitutively produced by the human glioma U 105MG cell line.

MCP1 mRNA is induced in human peripheral blood mononuclear leukocytes by phytohemagglutinin (PHA), lipopolysaccharide, and IL1, but not by IL2, TNF or IFNgamma.

In mesangial cells the synthesis and release of MCP-1 is rapidly induced by IgG complexes, but not monomeric IgG or F(ab)2 fragments of IgG.

MCP-1 is chemotactic for monocytes but not neutrophils. Maximal induction of migration is observed at a concentrtion of 10 ng/ml. Point mutation have been described at two amino acid positions which alter the factor so that it is then also chemotactic for neutrophils.

Elevated levels of MCP-1 are observed in macrophage-rich atherosclerotic plaques. The factor activates the tumoricidal activity of monocytes and macrophages in vivo. It regulates the expression of cell surface antigens (CD11c, CD11b) and the expression of cytokines (IL1, IL6).

MCP-1 is a potent activator of human basophils, including the degranulation and the release of histamines. In basophils activated by IL3, IL5 or GM-CSF, MCP-1 enhances the synthesis of leukotriene C4, (LC4).

IL1, TNAalfa, PDGF, TGFbeta and LIF induce the synthesis of MCP-1 in human articular chondrocytes, which may thus play an active role in the initiation and progression of degenerative and inflammatory arthropathies by promoting monocyte influx and activation in synvial joints.

Muistiiin 28.3. 2019

Citate :
Horst Ibelgaufts. Dictionary of Cytokines. 1995 VCH. Winham, New York, Basel, Cambridge, Tokyo. Page 522-3.

MIF, Migration Inhibition factor, Macrophage migration inhibitory factor (MMIF).
An operational definition for factors that inhibit in vitro the migration of macrophages out of capillary tubes or small pieces of tissue.
Many proteins have been described to possess MIF activity, including TNF, IFN-gamma, IL1, IL2, GM-CSF , LIF leucocyte migration inhibitory factor.
The proteins known as MRP8 and MRP14 ( MIF-related protein) are MIF- related proteins that are recognized by some monoclonal antibodies directed against MIF- activities.
Another protein MIF-1, with MIF activity is secreted by T sell hybridoma,
Another poorly characterized migration inhibitory factor is FSMIF-2.
Another factor influencing the chemotactic behavior of neutrophilic macrophages is ”HDLF” ( Hodgin-derived leucocyte factor).
In addition there are many other poorly characterized factors with MIF activity that cannot be blocked by antibodies against known cytokines and that are therefore probably distinct factors.

MMIF, a major secreted protein released by anterior pituitary cells in response to bacterial LPS.
It is identical with Sarcolectin binding protein. Pituitary-derived MIF contributes to circulating MIF present in the post-acute phase of endotoxinemia ( see also. Septic chock).
Recombinant murin MIF greatly enhances lethality when co-injected with LPSs,
and anti-MIF antibodies confer protection against lethal endotoxinemia.

One particular factor with MIF activity is also found in chicken murine and human embryonic eye lenses ( see 10K protein). A 12kDa factor of 115 amino acids that also inhibits the migration of macrophages is produced by antigen-stimulated T cells.

These proteins show extensive seq homology with each other and with a rat liver protein , designed ”TRANSMIF”, a murine protein designated GIF (glycosylation inhibiting factor),
and a mouse delayed early responsive gene, designated ”DER6”.
These highly homol. prot. sharing seq. homol. up to 98%, are structurally related to the theta-class of GST, Glutathione S – transferase, a subclass of GSTs thought to be the most ancient evolutionary GST class. All proteins have retained a Glutathione (GSH) binding domaine and demonstrate transferase activity.
GSTs protect against xenobiotic chemicals by catalyzing the conjugation of glutathione (GSH), which renders them non-toxic.

MIF is known as a mediator of cellular immunity with specific effects on the differentiation of mononuclear phagocytes. The expression of MIF activity correlates well with delayed hypersensitivity and cellular immunity in humans and MIF is now recognized as a principal cytokine modulating T cell/macrophage interactions in the expression of delayed hypersensitivity and acquired cellular immunity.

Recombinant human MIF is responsible for the specific activation of macrophages to kill intracellular parasites such as Mycobacterium avium and Leishmania donovani.
Recombinant human MIF has been shown to activate macrophage expression of NO, a potent antimicrobial agent that is produced by the NO synthase (NOS) – mediated oxidation ot terminal L-arginine guanidine nitrogen atoms.
Recombinant human MIF upregulates expression of genes encoding HLA-DR and IL1 beta and elaboration of IL1beta by human monocyte-derived macrophages.
Human recombinant MIF can also activate cultural human peripheral blood monocytes and monocyte-derived macrophages to become cytotoxic for tumor cells in vitro.
MIF also induces macrophages to produce TNF-alfa and IL1beta.

Administration of soluble bovine serum albumin of human immunodeficiency virus 120 kDa glycoprotein to mice in the presence of recombinant MIF together with incomplete Freund´s adjuvant induces a strong T cell proliferative response comparable to that of complete Freund´s adjuvant.
Recombinant MIF also increases antibody production, especially IgG1 and IgM, in mice. MIF may be useful, therefore , as an adjuvant in the development of vaccines.
MIF activity can be detected in the synovia of patients with rhematoid arthritis.
The expression of MIF at sites of inflammation also suggest a role for the mediator in regulation the function of macrophages in host defence.

Muistiin 28.3. 2019

This means  that it is needed  again a new  large range  developmental work for a new  influenza vaccine  also for humans.  There is a  bird vaccine for  chickens, which helps them.  This  new virus has been  quite affecting to those people who  have been getting it.   This  epidemic  is  pandemic type, that means: a unique  and  novel virus in the question.   Altogether – this situation shall  catch  much of the global  budget  and concern  again, exact  as the pandemic   H1N1 some years ago.  Very important   is the preventive knowledge about the  dangers.   Old human vaccines have not these antigens H7 or N9, according what I guess.  Very important to know  which part of  human body is the target of its attack.  It seems so that  it  hits multiorgan way –  affecting  also  the cells of  natural immunity ( leucocytes, lymphocytes and thrombocytes- so  aspirin type medicin is  not  to recommendate, because  there  is even thrombocytopenia , not only leucopenia and lymphopenia.  So one have to be very  hygienic- nearly as in leucemia- or  radioactivity  accident,   for not to miiss  the native immune cells too much.   Also – I think- it is good to  reduce  biogen amines in the  food, because too much histamine ( and serotonin, tyramine, tryptamine) and other  biogene amines in food    also  makes immune cells  too briittle.  The radioactivity also   makes  histamine of the  immune cells  to  be released   in too big amounts  (  = radioac  sickness symtoms)  and make the cells to  disappear   because they become too  brittle .  So perhaps antihistamine  is useful. I personally  feel  concern for the leucosytes, because   my glutenintolerance began 1981  with lymphopenia and leucopenia and thrombocytopenia-  One  doctor gave me  advixce to  reduce the biogene amines of the food and to use Lomudal G.I. against histamine colics – even such kind of allergic  laryngeal spasms it was  a help.

The reservoir for this novel virus remains unknown, although a continuous co-circulation of multiple A(H9N2) genotypes in farmed poultry over a longer time might be responsible for antigenic changes and adaptation to chickens [2]. Experimental data have shown that susceptibility and transmission, as well as shedding of the virus in birds, is dependent on the bird species [3]. Evolution of A(H7N9) viruses in the poultry population since 2013 has resulted in a genetic heterogeneity across different regions in China [4].

(from abstract, results)

Lymphopenia, elevated aspartate aminotransferase, alanine aminotransferase, C-reactive protein and lactate dehydrogenase were common features, with higher incidences of leukopenia and thrombocytopenia in the LP group.

The acute phase of both groups (LP, HP)  was accompanied with elevated cytokines associated with disease severity, including MIF, MCP-1 and IP-10. Diffuse exudation of the lungs and consolidation were observed from all patients. The dynamics of virus shedding and PaO2/FiO2 were similar between both groups. Notably, a higher prevalence of neuraminidase inhibitors (NAIs) resistance in the HP-H7N9 virus was found.


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