About LD-78 Beta / CCL3L1:
Mechanism
LD78 is sometimes known as CCL3L1, which is also the name of the gene that encodes it. The gene is of particular interest to a number of areas of scientific study.
● The number of CCL3L1 genes that an individual possesses is incredibly varied. It has been found that CCL3L1 is found in higher numbers in people of African descent.
● The lowest average number of CCL3L1 genes is found in people of European descent.
● It is believed that susceptibility to the Human Immunodeficiency Virus (HIV) may be related to the numbers of CCL3L1 genes a person has.
Structure
The CCL3L1 gene consists of:
● 3 exons
And spans:
● Around 1.9 kb
Function
● LD78/CCL3L1 has one of a number of chemokine genes which are found on chromosome 17. It has long been known that chemokines are a wide family of proteins, who play key roles in a number of bodily functions. Most commonly, they are associated with their role in inflammatory response and immunoregulatory processes.
● More specifically, it is known that chemokines attract lymphocytes to areas of the body that are suffering from infection or damage.
● Furthermore, LD78 — like other chemokines — binds to chemokine receptors, including CCBP2 (or B6) and CCR5.
● The latter is particularly noteworthy, as CCR5 is a co-receptor for HIV. It has been found that the binding of LD48 to CCR5 may be able to inhibit the entry of HIV.
● Despite the fact that CCL3 and CCL3L1 are almost over 95% identical to one another, it has been noted that CCL3L1 is 30 times more potent are inhibiting R5 HIV-1.
Significant notes
In terms of clinical study, few studies have focused specifically on LD78 or on the CCL3L1 gene. However, there has been notes regarding the potential role it has to play for people who are suffering from HIV. This has been touched on above, and is related to the LD48’s role in binding to CCR5 to inhibit the entry of HIV. Additionally, this binding causes the receptor to experience endocytosis and may cause the receptor to be reprocessed and re-expressed.
These known facts have lead to intriguing theories and studies into the relationship between LD48 and HIV. It has been noted that the copy number of CCL3L1 varies among individuals. There are theories as to why this may be the case, including theories regarding segmental duplication.
It has been found that the vast majority of individuals have between one and six copies of the diploid genome. The more copy numbers, the more CCL3L1 is present, and thus the higher the level of competition for the CCR5 binding site. It has been found that the higher the level of competition at this site, the slower the advancement of disease in individuals who are confirmed to have active HIV infections.
The potential questions that LD78 and CCL3L1 pose in regards to research into HIV definitely make this little-known gene, and the protein it secretes, more intriguing.