From the combination of knowledge and actions, someone can improve their skill and ability. It will lead them to live and work much better. This is why, the students, workers, or even employers should have reading habit for books. Any book will give certain knowledge to take all benefits. This is what this the interferon system tells you. It will add more knowledge of you to life and work better. Try it and prove it.

The Interferon System

http://www.naturaleater.com/Science-articles/Commensal-bacteria-killer-cells.pdf

Priming of Natural Killer Cells by Nonmucosal Mononuclear Phagocytes Requires Instructive Signals from Commensal Microbiota

CONTROVERSY has surrounded the role of the normal microbial flora in health since the early days of microbiology. Pasteur, for one, hypothesized that the normal flora was essential to life.1 Some years later, his hypothesis was tested and convincingly refuted by Reyniers and others at the Lobund Laboratory, University of Notre Dame, who demonstrated that the germ-free state could be maintained for successive generations in various laboratory animals.2 Metchnikoff, in one of many differences with Pasteur, argued that indigenous microorganisms were antagonists that competed with the host for factors essential to life.3 Metchnikoff's proposal has not been so easily rejected. . . .

The normal microbial flora.

The Sendai virus (SeV) V protein is characterized by the unique cysteine-rich domain in its carboxy-terminal half which is fused to the amino-terminal half of the P protein, but its function has remained enigmatic. The V protein-directing mRNA is generated by a remarkable process known as mRNA editing involving the pseudotemplated addition of a single G residue at a specific septinucleotide locus in the P gene, whereas the unedited exact copy encodes the P protein. Here, we introduced two nucleotide changes in the septinucleotide motif (UUUUCCC to UUCUUCC) in a full-length SeV cDNA and were able to recover a virus from the cDNA, which was devoid of mRNA editing and hence unable to synthesize the V protein. Compared with the parental wild-type virus with regard to gene expression, replication and cytopathogenicity in various cell lines in vitro, the V(-) virus was found to be either potentiated or comparable but never attenuated. The V(-) virus, however, showed markedly attenuated in vivo replication capacity in and pathogenicity for mice. Thus, though categorized as a nonessential gene product, SeV V protein encodes a luxury function required for in vivo pathogenicity.

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The paramyxovirus, Sendai virus, V protein encodes a luxury function required for viral pathogenesis.

Human natural interferon-α producing cells

Temperature-sensitive phenomenon of viral maturation observed in BHK cells persistently infected with HVJ.

BHK-HVJ cells, a cell line of baby hamster kidney cells persistantly infected with HVJ (Sendai virus), started to produce infectious virus by shifting down the incubation temperature from 38 to 32 C. The virus derived from BHK-HVJ cells, designated as HJV-pB, was effectively neutralized with antibody against wild-type virus (HVJ-W) which was used for the establishment of BHK-HVJ cells. HVJ-pB replicated in eggs at 32 C, but not at 38 C, while HVJ-W grew equally well at both temperatures. When BHK cells infected with HVJ-PB were incubated at 38 C, production of infectious virus, hemagglutinin, and neuraminidase was markedly restrained, whereas a considerable amount of viral nucleocapisid and envelope antigens was detected in the cells by complement fixation tests. These viral activities became detectable immediately after temperature shift-down from 38 to 32 C even at the later stage of infection. HVJ-pB was indistinguishable from HJV-W with respect to particle size, density, and morphological characteristics, but appeared to possess a higher neuraminidase activity and was inactivated more rapidly at 50 C than HVJ-W. HVJ-pB was less cytocidal and could easily cause latent infection in BHK and mouse L cells.

Temperature-sensitive virus derived from BHK cells persistently infected with HVJ (Sendai virus).

The present study was aimed to clarify the pathogenesis of Sendai virus infection to the central nervous system (CNS) of mice. One-to 2-day-old suckling and 4-week-old mice were inoculated intracerebrally with the virus. The virus multiplied higher in suclings than in adults. Immunofluorescent studies in sucklings revealed that the viral antigens appeared initially in ependyma, choroid plexus epithelium, and meninges. Subsequently they spread to subependymal cells and finally were found in neurons of hippocampus for as long as 4 months postinfection. In adults, however, the viral antigens rapidly disappeared in the early stage. Most mice inoculated intracerebrally with Sendai virus appeared healthy, although hydropcephalus developed in a few mice. Virus-specific antibody and interferon production seemed to have no influence on the persistent infection of Sendai virus in the CNS of mice. One of the most significant findings may be that the viral antigens persist in the brain for as long as 4 months in a latent form. This may offer a useful model for the study of latent CNS infection of paramyxoviruses.

https://iai.asm.org/content/iai/13/5/1497.full.pdf

Yasuhiko Ito

Papers

Temperature-sensitive phenomenon of viral maturation observed in BHK cells persistently infected with HVJ.

Temperature-sensitive virus derived from BHK cells persistently infected with HVJ (Sendai virus).

Pathogenesis of Sendai virus infection in the central nervous system of mice.

Production of interferon-like substance by mouse spleen cells through contact with BHK cells persistently infected with HVJ.

Mechanism of endotoxin-type interferon production in mice.