COVID-19

COVID-19

Again, I think it is good to have some idea what patients are going through with this virus. You, as well as I, may not understand all the complexities of this disease, but I feel it good to understand as much as possible. It is my wish and prayer for your families to stay safe from this virus, and the ones who have had to deal with it, a fast and complete recovery.

Pathologic examinations revealed lungs of patients with COVID-19 exhibited edema, proteinaceous exudate, focal reactive hyperplasia of pneumocytes with patchy inflammatory cellular infiltration, and multinucleated giant cells. Multinucleated giant cell formations can arise from numerous types of bacteria, diseases, and cell formations. Giant cells are known to develop when infections are also present.

In the process of giant cell formation, monocytes or macrophages fuse together, which could cause multiple problems for the immune system. Hyaline membranes were not prominent. Hyaline membranes are membranes composed of proteins and dead cells, which line the alveoli (the tiny air sacs in the lung), making gas exchange difficult or impossible. These changes likely represent an early phase of the lung pathology of COVID-19 pneumonia.

As time goes on patients have difficulty in breathing, chest tightness, wheezing, and dry cough, in the context of a diagnosis “suggestive of viral pneumonia,” with intermittent peripheral capillary oxygen hypoxia. With some patients, despite comprehensive treatment, including antibiotics, assisted oxygenation, and other supportive care, the patient’s condition deteriorates. At this point the patient will start to show prominent inspissated spherical secretions, focal fibrin clusters mixed with mononuclear inflammatory cells and multinucleated giant cells in the airspaces.

Other pathologic findings include edema and prominent proteinaceous exudates, vascular congestion, and inflammatory clusters with fibrinoid material, reactive alveolar epithelial hyperplasia, fibroblastic proliferation (plugs), and acute lung injury, such as edema, inflammatory infiltrate, type II pneumocyte hyperplasia.

Both high white blood cell counts and lymphocytopenia are consistent with COVID-19, may be a good clue for early diagnosis. This process takes days to occur. Researchers say, even among patients who do present with fever, commonly used pharyngeal swab PCR tests may still be negative, they suggested, due to the lack of virus in the upper respiratory tract, and despite the presence of pneumonia.

The COVID-19 virus contains an internal helical RNA-protein nucleocapsid surrounded by an envelope containing viral glycoproteins. Nucleocapsid protein is a phosphoprotein that is complex with genome RNA to form the nucleocapsid. Spike glycoprotein forms the large glycosylated peplomers that are characteristic of coronaviruses. A capsid is the protein shell of a virus. The capsid of the COVID-19 virus encloses the RNA nucleic acid.

For the coronavirus to replicate, the following has to occur. After receptor interaction and fusion of viral and plasma membranes, virus-specific RNA and proteins are synthesized, probably entirely in the cytoplasm. Expression of coronaviruses starts with translation of two polyproteins, pp1a and pp1ab, which undergo cotranslational proteolytic processing into the proteins that form the replicase complex. This complex is used to transcribe a 3′-coterminal set of nested subgenomic mRNAs, as well as genomic RNA, that have a common 5′ “leader” sequence derived from the 5′ end of the genome. Proteins are translated from the 5′ end of each mRNA. New virions are assembled by budding into intracellular membranes and released through vesicles by the cell secretory mechanisms. RER, rough endoplasmic reticulum; ER/GIC, endoplasmic reticulum/Golgi intermediate compartment.

Spike proteins are representative of those of all group I to III coronaviruses and of SARS-CoV. The coronavirus spike protein is synthesized as a precursor, cotranslationally glycosylated, and, in some cases, cleaved in the approximate middle into S1 and S2 subunits at a site with dibasic amino acids (BBXBB). S1 forms the external domain containing the receptor-binding domain (RBD) at its 5′ end, followed by, in the case of MHV, a hypervariable domain (HVR). A short signal sequence in cleaved from the 5′ end of the mature protein. S2 is the transmembrane subunit containing two heptad repeats (HR1 and HR2) and the transmembrane (TM) domain.

Interferons are a group of signaling proteins made and released by host cells in response to the presence of viruses. In a typical scenario, a virus-infected cell will release Interferons, causing nearby cells to heighten their anti-viral defenses.
C19 has encode numerous genes that allow for successful evasions of the host immune system.

In the immune system, effector cells are the relatively short-lived activated cells that defend the body in an immune response. Effector B cells are called plasma cells and secrete antibodies, and activated T cells include cytotoxic T cells and helper T cells, which carry out cell-mediated responses. Viral load, also known as viral burden, viral titre or viral titer, is a numerical expression of the quantity of virus in a given volume. It is often expressed as viral particles, or infectious particles per ml.

Though Covid-19 often begins as an upper respiratory tract infection, with cough and sore throat, coronavirus can trek down the throat and enter the lower respiratory tract. There, it damages the lung’s tiny air sacs, called alveoli, which are where oxygen enters the blood and carbon dioxide leaves.

As a result of this damage, inflammatory cells and fluid flood the alveoli. This makes it harder for oxygen to travel from the lungs into the bloodstream and deprives the organs of the oxygen that is necessary for them to function. You might hear this referred to as acute respiratory distress syndrome, or ARDS, which is a term for rapid and extensive lung damage that compromises the body’s oxygen supply during a severe pneumonia.

The decision to intubate is when the lungs are so damaged that a patient is not getting enough oxygen, because the ventilator can provide more oxygen to the body than a nasal cannula (nose prongs) or a face mask. In order to connect a patient to the ventilator, pain-relieving meds are given, and then an endotracheal tube is place into the trachea. The ventilator is not a treatment to heal damaged lungs but instead allows the lungs a longer time to recover on their own.

To try to minimize further damage, selected settings on the ventilator are tailored to the patient respiratory demands, usually smaller volumes with faster rates. As a result, patients with ARDS are often deeply sedated in the early hours and days of their illness so that they are able to tolerate the ventilator. We might also give a drug to temporarily paralyze the patient’s muscles so that they do not move or fight against the ventilator, which could cause more lung damage. Additionally, the breathing tube itself can be uncomfortable, causing gagging, coughing and nausea, so we use sedating medications to improve patient comfort.

When the patient is on the ventilator, a complete list of monitoring criteria is followed, including critical measurements such as oxygen, carbon dioxide, heart and kidneys. Some hospitals have dedicated rotating beds to aid in perfusion and oxygenation. Rotating beds can also help in secretion control. This works by changing how blood flows through the lungs, so it doesn’t pool with gravity in the collapsed bottom of the lungs. It has been found prone positioning reduces mortality in severe lung failure.

If a patient has been on a vent for two weeks, a tracheostomy tube, a plastic tube in the neck becomes indicated that offers a more permanent connection to the ventilator. The endotracheal tube can do damage to the vocal cords if left in for more than about two weeks, so the tracheostomy, or “trach,” allows more time for the lungs to recover, while avoiding damage to the vocal cords, plus the endotracheal tube also makes it easier to suction secretions. During this period of recovery, the patient may be moved to a more long-term care unit. After recovery, other issues such as anxiety, depression, post-traumatic stress, even cognitive dysfunction must be monitored.

In certain patients with COVID-19, the virus infection causes pneumonia and severe inflammation that cripples the lung’s function. In these patients, having a ventilator available to support the patient can make the difference between life and certain death.

The coronavirus causes acute lung injury and acute respiratory distress syndrome (ARDS). A person must have an effective immune response. There is 50% mortality in the aged and immunosuppressed populations. Many patients who make it off vents suffer from long-term physical, mental and emotional issues, such as post-traumatic stress disorder, Alzheimer’s-like cognitive deficits, depression.

When C19 patients are in the hospital for long periods of time, don’t forget they have been isolated at the bedside for the lack of visitation and can have “ICU Delirium”, meaning they become confused and may have nightmarish hallucinations. With social distancing, rehabilitation services are limited at this time. It can be a long road to recovery even after hospitalization for the lack of rehab care.

Bonefish

still don't think it came from a bat.

There are number of theories as to how this virus started. One is the bat theory. Then there is the Wuhan live animal market theory. Next, is the escape from a Wuhan biological lab theory. Most likely, we will never know how it started. However, whether this virus was manipulated or if it mutated in the animal host or if it mutated once it entered a human, it is a human cell destroyer. This virus has the potential to be a problem for years to come, if it is not stopped from mutating and being transmitted.

I listened to Senator John Kennedy, and the following is what he has to say about the origins of the virus. The Chinese high containment lab in Wuhan had been working on a bat virus for sometime. Kennedy believes this virus got out of the lab. Scientists around the world were predicting this escape an accident ready to happen two years ago. Since this virus’ escape, China has refused to let anyone speak to those in the lab or the people first infected. The doctors and reporters have disappeared from public access. Kennedy said China is needs to start cooperating in sharing genetic material and interviewing the people involved, but not to hold your breath. Kennedy, in his colorful way of saying things said, “China will steal the hair off you head and eat your lunch and bag that comes with it.” I love this Guy!

It is also found the coronavirus attacks hemoglobin in the red blood cells through a series of cellular actions, ultimately renders the red blood cells incapable of transporting oxygen, causing so-called ARDS symptoms. Red blood cells are critical oxygen carriers to the various cells in the body. Inside the red blood cells is a molecule called hemoglobin that contains “heme groups.” Each of these “heme groups” is a molecular “ring” known as “porphyrin” that holds an Iron ion or FE ion. It is the FE ions, which helps to transport oxygen in the bloodstream depending on states of oxidation. Typically the red blood cells pick up oxygen from the lungs to transport to other parts of the bodies.

Once inside a human host cell, the virus’s RNA also codes for a number of non-structural proteins that are created during the replication process. These proteins are not part of the virus itself but helps the virus to ‘hijack” other cellular pathways or actions to facilitate its survival in the host. The research discovered that some of these proteins hijack the red blod cells and remove the Iron ions from the “heme groups” and replace themselves with it. This makes the hemoglobin unable to transport oxygen. As a result, the lungs are stressed out and inflamed while the rest of the organs are also being affected. The so-called ARDS and subsequent organ failure could be attributed to this.

It was also suggested by another virologists that perhaps the coronavirus does not produce these proteins in the early stages of infection but will do so as a certain threshold is reached. This could explain the observations made by ER doctors that patients tend to have elevated ferritin. Typically ferritin is used to store excess iron. If a lot of iron is “pushed” out of “heme groups” and circulating around, the body produces more ferritin. Many ER and ICU doctors are now questioning treatment protocols and also questioning the usage of ventilators in certain cases.

bio-weapons are the perfect weapon, even better than chemical weapons.
they don't get an immediate response from the targeted country.
shuts down the targeted country.
makes offensive weapons useless if not used immediately by sickening military staff.
very cheap to make and replenishes itself.

this may have been a mistake but even so, china should pay dearly.
if we ever find this came from that lab, we should melt wuhan.

i'm assuming nuclear heat will kill the virus that escapes from the explosion.

i deal with chinese for business.
they have no soul. never trust a chinaman.
they will cut your throat and never bat an eye.

The following excerpts were from Fox News this evening.

Scientists at BSL-4 labs, like the one in Wuhan, typically work with agents or diseases that are extremely dangerous and can cause death to humans. Since opening, Wuhan lab has studied SARS, Ebola, HIV, West African Lassa virus and COVID-19, the disease caused by coronavirus. It works in collaboration with different universities around the world such as Wageningen University in the Netherlands and Montpellier 2 University in France. It also has close ties to Texas and has been receiving assistance form the Galveston National Laboratory at the University of Texas Medical Branch as well as other organizations.

Foreign affairs expert Gordon Chang said in a recent opinion piece on Fox News that "many Chinese believe the virus either was deliberately released or accidentally escaped from the Wuhan Institute of Virology, a P4-level bio-safety facility." He added: "This lab, known for studying coronaviruses, is not far from the market that had been initially identified as the source of the outbreak."

"During interactions with scientists at the WIV laboratory, they noted the new lab has a serious shortage of appropriately trained technicians and investigators needed to safely operate this high-containment laboratory," the Jan.19, 2018, cable, written by two officials from the embassy's environment, science and health sections who met with the WIV scientists, said. The cable also called attention to Shi, the scientist who at first considered the virus might have gotten out of the lab accidentally but then backtracked.