Inoculation needle subcutaneously or intramuscular injection needle

Different methods of vaccination are different:

Oral: Polio vaccine (sugar pill), rotavirus

Intradermal injection: BCG vaccine

Subcutaneous INJECTION: RUBELLA VACCINE, MEASLES vaccine, MUMPS VACCINE, meningitis vaccine, JE vaccine, HEPATITIS A VACCINE, VARICella vaccine, MUMPS vaccine, LEPROSY vaccine, MUMPS vaccine, etc

Intramuscular injection (also called intramuscular injection) : DPT, diphtheria, hepatitis B, rabies vaccine, influenza vaccine

Others use different methods depending on the situation: for example, some flu vaccines are given intramuscular, subcutaneous or both. Inactivated influenza vaccines under development are administered either subcutaneously (or intramuscularly) or intranasally. And HIB is mostly intramuscular injection, some special circumstances (such as hemorrhagic disease to inject subcutaneously).

But the subcutaneous vaccine is relatively more.

This has nothing to do with Class I and Class II vaccines, the rabies vaccine is intramuscular like the Class I vaccine; Measles is a Class I vaccine but you still have to give it subcutaneously.

2. How does the virus infect nerve cells

So how does the novel coronavirus infect nerve cells? The ACE2 receptor is known to be a deliberate binding site for the novel coronavirus, but its mRNA expression is relatively low in the nervous system. The team found low levels of ACE2 expression in all 31 cell populations by single-cell sequencing.

However, ACE2 protein expression is more in a variety of nerve cells, such as MAP2-positive nerve cells showing a relatively high level. These results indicated that there was no direct relationship between ACE2 transcription level and protein expression level.

Therefore, it is highly likely that the virus still invades nerve cells through ACE2 receptors. To demonstrate the test, the team extracted cerebrospinal fluid (CSF) from COVID-19 patients containing neutralizing antibodies and incubated it with organoids, finding that it effectively reduced organoid infection by COVID-19.

To further investigate the effects of SARS-CoV-2 on the CNS in vivo, the team turned to humanized ACE2 transgenic mice and found by immunofluorescence that SARS-CoV-2 was widely distributed in multiple brain regions 7 days after infection (FIG. 2A-E).

By directly expressing ACE2 receptors in the brain and infecting the coronavirus with AAV-HAEC2, the team found that brain infection alone induced weight loss and death in mice, even when the dose was only one hundredth of that of lung infection (Figure 2H-J).

The authors pointed out that nerve infection of the novel coronavirus is one of the important causes of death from the novel coronavirus. Previous studies have shown that specific overexpression of the ORF3a protein in Drosophila brain promotes neuroapoptosis, neuroinflammation, and death, but the strongly pro-apoptotic protein NSP1 does not have similar neurotoxicity. Therefore, it is still an important problem in front of us to study the molecular mechanism of specific neurological disorders induced by COVID-19. The team's model of organoid and mouse brain infection suggests a feasible technical approach to this question.

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