Human immunodeficiency virus (HIV) is a lentivirus that infects cells of the human immune system and is a type of retrovirus. It is generally believed that human immunodeficiency virus infection leads to AIDS, a disease in which acquired cellular immune function is defective and causes severe random infection and/or secondary tumor death. HIV originated in Kinshasa, Africa in the 1920s and was recognized and developed into a global pandemic in the United States in 1981. Human immunodeficiency virus is also commonly known as "HIV" or "HIV."

Human immunodeficiency virus, as a retrovirus, integrates into the genome of the host cell after infection, and current antiviral therapy does not eradicate the virus. In 2016, the World Health Organization (WHO) estimated that there are about 36.7 million people living with HIV worldwide [1]. The most prevalent is sub-Saharan Africa, followed by South Asia and Southeast Asia. The fastest growing region is East Asia. Eastern Europe and Central Asia.

In some periods of the course of human immunodeficiency virus infection, especially early and late stages, infectious viral particles may be present in certain body fluids containing immune cells, plasma, lymph or tissue fluids, such as blood, semen, prostatic fluid, Vaginal secretions, milk or wound secretions; on the other hand, the virus is extremely unstable in an in vitro environment. Therefore, the path of human immunodeficiency virus transmission is mainly unsafe sex, intravenous injection, blood transfusion, childbirth, breastfeeding, etc.; usually work, study, social or family contact, such as contact between intact skin, shared toilet, contact Sweat, etc., does not transmit human immunodeficiency virus; normal contact with saliva or tears (such as social kisses or short kisses) does not lead to the transmission of human immunodeficiency virus; but the US Centers for Disease Control and Prevention says it has been infected with the virus. The mother can pass the virus to the child through the food that has been chewed first (the blood contained in the saliva).


The human immunodeficiency virus infects a variety of cells, including CD4-positive helper T cells and macrophages, which express CD4 molecules on the surface. The entry of a virus into a helper T cell or macrophage is not only mediated by the interaction between the glycoprotein gp120 of the viral particle envelope and the CD4 molecule of the infected cell, but also requires a chemokine receptor on the surface of the host cell. Come as a synergistic receptor. Macrophage (M)-tropic human immunodeficiency virus (or non-syncitia-inducing strains, NSI) utilizes beta-chemokines (beta) -chemokine) Receptor CCR5 enters cells and can therefore replicate in macrophages and CD4-positive helper T cells. T cell (T)-tropic human immunodeficiency virus (or syncitia-inducing strains, SI) uses alpha-chemokine receptors because It replicates mainly in CD4-positive helper T cells, although it can also replicate in macrophages. A virus that enters cells only using the CCR5 receptor, called R5; a tube that uses only the CXCR4 receptor, is called X4; and both use it, it is called X4R5. Of course, depending on the type of co-receptor does not necessarily distinguish the actual cellular tropism of the virus.

Human immunodeficiency virus can also infect dendritic cells.

The interaction of glycoprotein gp120 with its co-receptor and CD4 molecule triggers a change in the conformation of gp120 protein, thereby exposing the originally buried part of the transmembrane glycoprotein gp41, thereby bringing the V3 loop of gp120 close to the co-receptor, and then gp41 leads to the virus. The fusion of the envelope with the target cell membrane allows the viral nucleocapsid to enter the cell. The specific mechanism by which gp41 causes cell membrane fusion remains unclear.

Some people are more resistant (but not completely resistant) to HIV because their cells lack a co-receptor for HIV entry into the cell. This synergistic receptor is the chemokine receptor CCR5. Their CCR5 gene has a 32-base long deletion, causing the product protein to be truncated and not detectable on the cell surface. These people are mainly distributed in Europe, but also in the Middle East and the Indian subcontinent.

As a virus, HIV must enter the cell to continue its life history (integration, replication, release...) and history of infection. The virus interacts with the cell membrane of the target cell and enters the cell through the gp120 glycoprotein on its surface and the CD4 molecule of the cell differentiation antigen (or differentiation cluster) on the surface of the target cell. This process requires a seven-transmembrane G-protein coupled receptor on the surface of the target cell. Currently found mainly the chemokine receptor CCR5 (M-type virus strain) and CXCR4 (T-like strain).

People with this CCR5 deletion, because the cell surface does not express CCR5, prevents part of HIV from entering and infecting such cells. But HIV can infect such cells through other co-receptors, or other types of cells can be infected without this CCR5, so these people are not completely resistant to HIV. In fact, there have been reports of HIV infection in homozygous individuals with this CCR5 deficiency.

Once the viral nucleocapsid enters the cell, the viral reverse transcriptase releases the virus's single-stranded sensed RNA from the viral protein and reverse transcription based on the sense RNA to generate the antisense complementary DNA (cDNA). This reverse transcription process is very error-prone, so this is an important step in the virus's mutation (eg, obtaining resistance). Then, double-stranded viral DNA (vDNA) is synthesized based on the cDNA. The new viral DNA is transported into the nucleus and integrated by the viral integrase into the genome of the host. In this way, the virus completes the infection and begins to enter the incubation period.

To start the virus, some transcription factors need to be present in the cells. The most important one, called NF-κB, is present in all activated T cells. This means that the cells that are most easily killed by the human immunodeficiency virus are precisely the cells that are involved in the infection.

Pathogenic mechanism

HIV selectively invades cells bearing CD4 molecules, mainly T4 lymphocytes, monocyte macrophages, dendritic cells, and the like. The cell surface CD4 molecule is an HIV receptor, which is mediated by gp41 through the HIV envelope protein gp120 and is mediated by gp41 to penetrate into susceptible cells, causing cell destruction.

Gp120 is a capsid protein of the HIV virus, encoded by the gene env, which has a molecular weight of 120 kD. It plays an important role in the process of virus invading human T cells. At the same time, it also exists in a free form, which enhances the non-specific activation of some major immune cells in vivo through a pathway similar to superantigen action. The harmful effects of HIV on the human body.

In the process of HIV invading the human body, gp120 expressed on the surface of the virus allows the HIV virus to easily bind to specific T lymphocytes, and then fuses with the T cell membrane through the outer shell of the viral protein to achieve the purpose of infecting T cells. In addition, gp120, which is free in the body, activates excess T cells through its special superantigen, and stimulates a series of reactions of other immune cells in the body, greatly reducing the immune function of the human body. Now the research on gp120 is gradually deepening, and it is foreseeable that gp120 will become a target molecule in AIDS immunotherapy in the near future.

There are several reasons why HIV is difficult to deal with. First, HIV is an RNA virus that uses reverse transcriptase to integrate RNA into the DNA of cells. In between, it has a lot of chances of mutation. Therefore, the virus will soon become resistant to therapies. Second, the idea that HIV is generally considered a T cell killer is not correct. If HIV is a killer virus, it will soon die because there is no more time to infect new infected people. Usually, HIV lives in the human body for several years and spreads through sexual activity or blood exchange without the patient's knowledge. It integrates itself into the DNA of the host cell and remains dormant for years, and the immune system does not respond to it because it is just a DNA fragment. When the cells divide and replicate, the virus is replicated together. After a few years, the virus becomes active, taking control of the cells and starting to replicate. In recent years, the notion that CD4+ T cells are directly reduced by HIV infection has also been questioned. The protein icing of HIV is driven by viral particles that fill the blood with these proteins, which stick to CD4+ T cells and bind them together. On the other hand, these cells are recognized by the immune system and cause an immune response that causes the immune system to kill its own CD4+ T cells.



The right condom can greatly reduce the chance of contracting HIV, but it is not seamless.

Post-Exposure Prophylaxis (PEP) for exposure to HIV: After exposure to infection (such as risky sexual behavior, needle sticks or other blood and body fluid exchange exposure), take anti-HIV drugs within 72 hours (per The second course of treatment (28 days) can effectively reduce the risk of HIV infection. [twenty two]

Treatment as Prevention: Infected people taking AIDS drugs have an excellent effect on preventing transmission, and seropositive ones in serum dissimilar partners can take a stable medication to avoid transmitting the virus to one of the negative parties. [twenty three]

Exposure to HIV Pre-Exposure Prophylaxis (PREEP): The use of anti-HIV drugs before exposure to HIV risk can also significantly reduce the chance of infection during the course of taking. [24] Currently, the drug for PrEP is only one of Shufatai, which is divided into daily doses or may be event-driven. For HIV sero-dissimilar partners, if one of the negatives is taken daily, the effect of avoiding HIV infection can reach 100%. [25][26]


Today patients are attacking HIV at different stages by taking different drugs. These drugs include:

Inhibition of proteases inhibits the activity of proteases required for HIV activity. It can also be used to suppress replication activities. Such as Saquinavir, Indinavir, Ritonavir, Kaletra, Nelfinavir and other drugs.
Inhibition of reverse transcriptase inhibitors (RTIs) inhibits reverse transcriptase activity. Reverse transcriptase is an enzyme used by HIV to replicate. The lack of this enzyme prevents HIV from building RNA and DNA. It comes in three forms:
Non-nucleotide reverse transcriptase inhibitors such as Nevirapine, Efavirenz, etc.
Nucleotide reverse transcriptase inhibitors such as zidovudine (AZT), stavudine (d4T), Didanosine (ddI), Zalcitabine (ddC), lamivudine 3TC), Abacavir (AZT+3TC)
Inhibition of entry of the drug inhibits AIDS by entering the cell by lysing the membrane of the host cell.
There are many difficulties in establishing a topic for HIV therapy. Every effective drug has side effects, usually severe or fatal. Common side effects include severe nausea, diarrhea, liver damage and failure, jaundice, hyperlipidemia, diabetes, adipose tissue shift, anemia, and kidney stones. Fatal side effects include Stevens-Johnson syndrome, violent hepatitis, pancreatitis, and lactate. Each treatment requires regular blood tests to determine efficacy and liver function.


Six methods of treating AIDS with Chinese medicine

1 lung and stomach suffering from evil syndrome: Xuanfei hurricane, clearing away heat and detoxification. Yinqiao powder plus earthworm, Prunella vulgaris.
2 lung and kidney yin deficiency syndrome: nourish lung and kidney, detoxification and phlegm. Lily Gujin Decoction, Melon, Fritillaria, Polygonum cuspidatum, Prunella vulgaris, Rhubarb, etc.
3 spleen and stomach weakness syndrome: Yongzheng evil, cultivated the spleen and stomach. Buzhong Yiqi Decoction combined with Shenqi Baizhu Powder plus soil mites, Tianji Huang, and cat claw grass.
4 spleen and kidney deficiency syndrome: warming the spleen and stomach, benefiting Qi back to Yang. Kidney gas pill contains Sishen pill plus pork chop, licorice and so on.
5 qi deficiency and blood stasis syndrome: qi and phlegm, live serum heat. Buyang Huanwu Tang, Xijiao Dihuang Decoction and Xiaoyu Pills add and subtract.
6: Medical Education Network collected and compiled Anfu Niuhuang Wan, Zi Xuedan, Zhibao Dan.
Western medicine treatment for AIDS
There is still a lack of effective drugs to eradicate HIV infection worldwide. The current treatment goals are: maximizing and lasting reduction of viral load; obtaining immune function reconstruction and maintaining immune function; improving quality of life; reducing HIV-related morbidity and mortality. The treatment of this disease emphasizes comprehensive treatment, including: general treatment, antiviral treatment, recovery or improvement of immune function treatment and treatment of opportunistic infections and malignant tumors.
General treatment
There is no need for isolation treatment for HIV-infected or acquired immunodeficiency syndrome patients. For people with asymptomatic HIV infection, they can still maintain normal work and life. Antiviral treatment should be based on the specific condition and closely monitored for changes in the condition. For patients with pre-AIDS or who have developed AIDS, they should pay attention to rest according to the condition and give a high-calorie, multi-vitamin diet. Those who cannot eat should be supplemented with intravenous infusion. Strengthen supportive therapies, including blood transfusions and nutritional support therapies, to maintain water and electrolyte balance.
2. Antiviral therapy
Antiviral therapy is the key to AIDS treatment. With the application of high-efficiency antiretroviral combination therapy, the efficacy of anti-HIV has been greatly improved, and the quality of life and prognosis of patients have been significantly improved.
The above is a comparison of the six methods used by Chinese medicine practitioners to treat AIDS and the methods of treating AIDS with Western medicine. I hope that the number of friends who need it can be understood. Xiaobian reminds AIDS patients not to give up their hopes of life, but also to build confidence. Family members also want to help AIDS patients regain their confidence in life.