Do White Blood Cells use Retroviruses for Cell fusions?
Alveolar macrophages (white blood cells) produce the Env protein of a human endogenous retrovirus, HERV-E 4-1, in a subgroup of interstitial lung diseases. http://www.ncbi.nlm.nih.gov/pubmed/9115754
Ok I'll try and explain where the research is going and why retroviruses are also likely to appear in white blood cells or macrophages in response to real infections of bacteria and fungi (the retroviruses being functional and already in the macrophage/WBC DNA.) The white blood cell monocytes or baby white blood cells join together into what they call 'giant cell multinucleated cells', this is in response to large infections, lots of dead cell debri, foreign bodies lodged in the body, anything that needs to be removed etc. So baby monocyte cells look like they join together into what I call "Giant death star white blood cells" or macrophages made of many immature white blood cell monocytes bound together with retroviruses creating cell fusions. TB and malaria are prime cases where giant cells are seen as a response to remove quite big bugs. "Macrophages undergo fusion with other macrophages to form the hallmark multinucleated giant cells of chronic inflammation. However, neither the existence of distinct morphological types of giant cells, the signaling pathways that induce their formation, the molecular mechanism(s) of macrophage fusion, nor the significance of macrophage multinucleation at chronic inflammatory sites are well understood. Our efforts have been focused on these unknowns, particularly as they relate to the foreign body-type giant cells that form on implanted biomaterials and biomedical devices"
Macrophage fusion and multinucleated giant cells of inflammation. http://www.ncbi.nlm.nih.gov/pubmed/21432016
It is also how bone and bone reformation is done, cell fusion is necessary, this also happens with eyes, muscles and more and we are only beginning to work it out.
Osteoclasts and giant cells: macrophage-macrophage fusion mechanism. http://www.ncbi.nlm.nih.gov/pubmed/11168677
Well it gets more interesting because tumours, leukemias and all autoimmune diseases express retroviruses, especially the very common HERV-K retrovirus which has been found in blood, muscle and more. HERV-K levels rise at the same levels of so called HIV in patients who get ill. HERV-K also appears in tumours where it is actually releasing env proteins and causing multinucleated cells, so the env in all our retroviruses is the same as the gp120 protein supposedly attributed to being a part of HIV, but all our retroviruses have envelopes or env proteins. So this is what they do, the retroviruses actually fuse cells together. sometimes that's needed, in the case of cancer it's not a good thing, with babies it's normal part of growing which is why kids have higher levels of retroviruses.
"Our results support the notion that proteins encoded by HERV K can mediate intercellular fusion of melanoma cells, which may generate multinuclear cells and drive the evolution of genetic changes that provide growth and survival advantages." 2013
Human endogenous retroviral K element encodes fusogenic activity in melanoma cells.
In the case of successful pregnancy the HERV-W retrovirus has to work so that the entire remodelling process of the uterus and blood supply and fetal attachment can occur so in experiments where they checked levels of the placental HERV-W retrovirus in pregnant women the lower levels of HERV-W retrovirus were indicative of failed pregnancies.
"Low Syncytin expression in both cultured cytotrophoblasts and primary tissues from pathological placentas supports an intrinsic placenta-specific deregulation of cell-cell fusion in the formation of syncytiotrophoblasts leading to increased apoptosis. These processes could contribute to the development and severity of Preeclampsia (PE), Hemolysis Elevated Liver Enzymes and Low Platelets (HELLP)-syndrome, and intrauterine growth restriction (IUGR)"
Impaired cytotrophoblast cell-cell fusion is associated with reduced Syncytin and increased apoptosis in patients with placental dysfunction.
When a wound happens retroviruses will even appear not only in normal cells but in the T-cells, this was a rather horrid 2013 experiment where they burnt mice and the retroviruses from the mouse genome start doing things at certain times post burning. Cell fusion and macrophage remodelling of collagen is all happening in wound healing, in the case of wounds the white blood cells are literally needed to dissolve old cells and get them out of the way to repair the damage. So retroviruses may fuse macrophages together and also fuse other cells, we are just learning now. "Murine leukemia virus-type endogenous retroviruses (MuLV-ERVs) constitute ~10% of the mouse genome and are associated with various pathophysiologic processes. In this study, we examined whether MuLV-ERVs’ response to burn-elicited stressors is specific for certain lymphocyte populations and/or locations of lymphoid organ.”
“MuLV-ERVs’ response to burn-elicited stressors may be differentially controlled depending on lymphocyte type, location of lymphoid organ, MuLV-ERV type, and stress duration.
Injury-elicited stressors alter endogenous retrovirus expression in lymphocytes depending on cell type and source lymphoid organ http://link.springer.com/article/10.1186%2F1471-2172-14-2
In another recent 2013 study the T-cells of people with Lupus were expressing retroviruses with hypomethylation of their DNA as well. Lupus is a potentially deadly autoimmune disease with symptoms that could easily get labelled as AIDS.
DNA methylation of human endogenous retrovirus in systemic lupus erythematosus.
So the T-cells of people with lupus have dysfunctional DNA and express retroviruses. Why should be the next question? Lupus studies have also shown consistently that up to one third of people with Lupus can look HIV+. So given that their T-cells are activated and showing retroviral activity what is the HIV antibody test actually detecting? If anything meaningful at all? "22 of 61 systemic lupus erythematosus (SLE) patients produced antibodies to the p24 gag protein of HIV-1 demonstrated by Western blotting." 1990
A conserved idiotype and antibodies to retroviral proteins in systemic lupus erythematosus.
"We have previously demonstrated that about one-third of patients with either Sjögren’s syndrome (SS) or systemic lupus erythematosus (SLE) react to human immunodeficiency virus (HIV) p24 core protein antigen without any evidence of exposure to, or infection with, HIV itself. " 1998
Reactivity of Sera from Systemic Lupus Erythematosus and Sjögren’s Syndrome Patients with Peptides Derived from Human Immunodeficiency Virus p24 Capsid Antigen
If you go back to the beginning and in light of what we know now about cancers fusing together with retroviruses then the symptoms of HTLV-III make more sense, patients had tumours forming and we also see the same phenomena in Multiple Sclerosis. "It has been postulated that the retrovirus HTLV-III/LAV thought to be the etiologic agent of AIDS also infects the central nervous system and directly causes AIDS encephalopathy. Electron microscopical studies performed on brain sections from three patients with AIDS complicated by progressive encephalopathy revealed structures morphologically consistent with HTLV-III/LAV retrovirus particles. The particles were located principally within multinucleated giant cells but were also present in astrocytes. Many particles were also noted in the extracellular space." 1983
HTLV-III/LAV-like retrovirus particles in the brains of patients with AIDS encephalopathy